Epilepsy is a complex neurological disorder aggravated by chronic neuroinflammation largely driven by reactive astrocytes.These cells promote epileptogenesis through persistent cytokine secretion and glial scar format...Epilepsy is a complex neurological disorder aggravated by chronic neuroinflammation largely driven by reactive astrocytes.These cells promote epileptogenesis through persistent cytokine secretion and glial scar formation.Current antiepileptic drugs remain ineffective in targeting these mechanisms due to limited blood-brain barrier(BBB)permeability and poor astrocytic specificity.A transferrin-functionalized biomimetic nanotherapeutic loaded with resveratrol(RN@RTA)was developed to regulate astrocyte-mediated inflammation by activating sirtuin 1(SIRT1)and suppressing the mitogen-activated protein kinase/nuclear factor Kappalight-chain-enhancer of activated B cells(MAPK/NF-κB)axis.Using in vitro BBB models,primary astrocytes,and a pilocarpine-induced chronic epilepsy mouse model,we evaluated the capacity of RN@RTA to cross the BBB,inhibit inflammatory signaling,and reduce seizure activity.Mechanistic assays included immunoprecipitation of NF-κB complexes,cytokine quantification,RNA sequencing,and histopathological assessments of glial and synaptic markers.RN@RTA achieved 82%uptake by hippocampal astrocytes and significantly reduced Il6,Tnf-α,and Nlrp3 expression.SIRT1 activation disrupted the NF-κB p65/p300 complex,leading to transcriptional repression of inflammatory genes and enhancement of autophagy.In vivo,seizure frequency decreased by 67%,synaptic structure was preserved,and astrogliosis was markedly alleviated.The findings demonstrate a dual regulatory mechanism in which RN@RTA suppresses neuroinflammatory signaling and restores neural homeostasis,offering a promising molecularly targeted approach for refractory epilepsy.展开更多
The objective of this research was to assess the potential of phosphatidylcholineencapsulated resveratrol as a cosmetic ingredient.The hydrogen peroxide(H_(2)O_(2))and ultraviolet A(UVA)induced human skin fibroblasts(...The objective of this research was to assess the potential of phosphatidylcholineencapsulated resveratrol as a cosmetic ingredient.The hydrogen peroxide(H_(2)O_(2))and ultraviolet A(UVA)induced human skin fibroblasts(HSF)models of skin damage were established to compare the antioxidant and anti-wrinkle properties between phosphatidylcholine-encapsulated resveratrol and unencapsulated resveratrol.The findings reveal that encapsulating resveratrol with phosphatidylcholine not only enhances skin absorption but also significantly improves its antioxidant capabilities.In the H2O2-induced HSF injury model,phosphatidylcholine-encapsulated resveratrol demonstrates a superior ability to neutralize reactive oxygen species(ROS)generated by H2O2 compared to the resveratrol group.Further analysis indicates that this enhanced functionality is associated with increased enzymatic activities of superoxide dismutase(SOD),glutathione peroxidase(GSH-Px)and catalase(CAT)when treated with phosphatidylcholine-encapsulated resveratrol.Additionally,in UVA-irradiated HSF cells,phosphatidylcholine-encapsulated resveratrol effectively reduces the levels of matrix metalloproteinases-1 and-3(MMP-1 and MMP-3)and increased the contents of CollagenⅠand CollagenⅢ(Col-1 and Col-3),demonstrating significant anti-wrinkle effects.These findings provide critical evaluation criteria and application references for enhancing cosmetic ingredients through phosphatidylcholine encapsulation,thereby advancing skincare formulations.展开更多
The dietary polyphenolic compounds resveratrol and quercetin prevent neurodegenerative diseases in experimental models;however, they reach the brain only in nanomolar concentrations in the glucuronidated and sulfated ...The dietary polyphenolic compounds resveratrol and quercetin prevent neurodegenerative diseases in experimental models;however, they reach the brain only in nanomolar concentrations in the glucuronidated and sulfated forms, and not as the aglycone parent form(Pasinetti et al.,2015).展开更多
Objective Resveratrol(Res)is a promising anticancer drug against hepatocellular carcinoma(HCC),but whether its anti-HCC effects implicate mitophagy remains unclear.Therefore,we aimed to explore the specific role of Re...Objective Resveratrol(Res)is a promising anticancer drug against hepatocellular carcinoma(HCC),but whether its anti-HCC effects implicate mitophagy remains unclear.Therefore,we aimed to explore the specific role of Res in mitophagy and the related mechanisms during the treatment of HCC.Methods HepG2 cells and tumor-grafted nude mice were used to investigate the effects of low-,middle-and high-dose of Res on HCC progression and mitophagy in vitro and in vivo,respectively.A series of approaches including cell counting kit-8,flow cytometry,wound healing and transwell assays were used to evaluate tumor cell functions.Transmission electron microscopy,immunofluorescence and Western blotting analysis were used to assess mitophagy.Mitochondrial oxygen consumption rate,reactive oxygen species and membrane potential were used to reflect mitochondrial function.After disrupting the expression of metastasis-associated lung adenocarcinoma transcript 1(MALAT1),miR-143-3p,and ribonucleoside reductase M2(RRM2),the effects of the MALAT1/miR-143-3p/RRM2 axis on cell function and mitophagy under Res treatment were explored in vitro.Additionally,dual-luciferase reporter and chromatin immunoprecipitation were used to confirm interactions between target genes.Results Res significantly inhibited the proliferation and promoted apoptosis of HCC cells in vitro,while significantly suppressing tumor growth in a dose-dependent manner and inducing mitophagy and mitochondrial dysfunction in vivo.Interestingly,MALAT1 was highly expressed in HCC cells and its knockdown upregulated miR-143-3p expression in HCC cells,which subsequently inhibited RRM2 expression.Furthermore,in nude mice grafted with HCC tumors and treated with Res,the expression of MALAT1,miR-143-3p and RRM2 were altered significantly.In vitro data further supported the targeted binding relationships between MALAT1 and miR-143-3p and between miR-143-3p and RRM2.Therefore,a series of cell-based experiments were carried out to study the mechanism of the MALAT1/miR-143-3p/RRM2 axis involved in mitophagy and HCC;these experiments revealed that MALAT1 knockdown,miR-143-3p mimic and RRM silencing potentiated the antitumor effects of Res and its activation of mitophagy.Conclusion Res facilitated mitophagy in HCC and exerted anti-cancer effects by targeting the MALAT1/miR-143-3p/RRM2 axis.展开更多
Aim To synthesize a new prodrug, resveratrol trinicotinate. Methods Inpresence of lithium and a catalytic amount of naphthalene, the reaction of p-methoxybenzyltrimethylsilyl ether and 3,5-dimethoxylbenzaldehyde gave ...Aim To synthesize a new prodrug, resveratrol trinicotinate. Methods Inpresence of lithium and a catalytic amount of naphthalene, the reaction of p-methoxybenzyltrimethylsilyl ether and 3,5-dimethoxylbenzaldehyde gave resveratrol after a series of translation.Resveratrol trinicotinate was obtained by the reaction of resveratrol and nicotinoyl chloridehydrochloride. Results A mutual prodrug resveratrol trinicotinate was designed and synthesized.Conclusion A novel method for synthesis of resveratrol and resveratrol trinicotinate has beenafforded. The E-isomer is selectivily obtained by dehydration of the compound 2 with KHSO_4 .展开更多
There is still no effective treatment for pancreatic cancer,one of the deadliest malignancies among the gastrointestinal diseases.Jiang et al demonstrated the presence of senescent cancer-associated fibroblasts(CAFs)i...There is still no effective treatment for pancreatic cancer,one of the deadliest malignancies among the gastrointestinal diseases.Jiang et al demonstrated the presence of senescent cancer-associated fibroblasts(CAFs)in pancreatic cancer tissues,supporting the use of CAFs as potential anti-cancer targets.The study indicated that a natural plant-derived compound resveratrol can reverse senescent CAF phenotype and decrease the growth,migration,and invasiveness of pancreatic cancer cells.Notably,the study indicated that resveratrol might be involved in regulating epithelial-to-mesenchymal transition in the tumor microenvironment.This editorial shares insights on the future investigation of resveratrol signaling in cancer cells and the tumor microenvironment,and discusses resveratrol-based treatment perspectives.展开更多
Emerging evidence highlights the potential of bioactive compounds,particularly polyphenols,as adjunctive therapeutic agents in the treatment of pancreatic cancer(PC),one of the most aggressive malignancies.This review...Emerging evidence highlights the potential of bioactive compounds,particularly polyphenols,as adjunctive therapeutic agents in the treatment of pancreatic cancer(PC),one of the most aggressive malignancies.This review focuses on epigallocatechin gallate(EGCG)and resveratrol due to their extensively documented anticancer activity,favorable safety profiles,and their unique ability to modulate multiple signaling pathways relevant to pan-creatic tumorigenesis.Among polyphenols,these two have shown superior anti-cancer activity,epigenetic regulatory effects,and synergy with standard chemotherapies in preclinical pancreatic cancer models.Resveratrol exhibits anti-proliferative effects by modulating key signaling pathways,including phosphatidylinositol 3 kinase(PI3K)/protein kinase B(Akt),nuclear factor kappa-B(NF-κB),and tumor protein 53(p53).EGCG exerts anti-cancer activity by targeting multiple cellular processes,such as oxidative stress reduction,and suppression of inflammatory mediators like Interleukin-6(IL-6)and Tumor Necrosis Factor-α(TNF-α).Both EGCG and resveratrol exert anti-pancreatic cancer effects partly through direct interactions with cell surface receptors and modulation of intracellular cascades.EGCG targets the 67 kDa laminin receptor(67LR),which is overexpressed in pancreatic cancer cells,triggering apoptosis,cyclic guanosine monophosphate(cGMP)production and activation of the PKCδ/acid sphingomyelinase(ASM)cascade.Resveratrol inhibits insulin-like growth factor-1 receptor(IGF-1R)activation of the PI3K/Akt and Wnt signaling pathways,while concurrently activating tumor suppressor p53.These interactions suppress proliferation,promote apoptosis,and reduce epithelial-mesenchymal transition(EMT),thereby limiting tumor progression.Both polyphenols enhance chemosensitivity and reduce resistance to conventional therapies,including gemcitabine,by modulating drug transporters and apoptotic pathways.Furthermore,their epigenetic influence,particularly via DNA methylation and histone modification,suggests a broader role in pancreatic cancer prevention.Understanding the roles and mechanisms of resveratrol and EGCG in pancreatic cancer provides valuable insights into novel treatment strategies.The integration of polyphenols into conventional therapeutic approaches may offer new hope for improving patient outcomes.展开更多
Background: Resveratrol is a widely recognized anti-inflammatory and antioxidant agent,and it has been suggested to possess anti-tumor effects. But the effect of resveratrol onhepatocellular carcinoma and its molecula...Background: Resveratrol is a widely recognized anti-inflammatory and antioxidant agent,and it has been suggested to possess anti-tumor effects. But the effect of resveratrol onhepatocellular carcinoma and its molecular mechanisms are unknown. This study confirmedthe effects of resveratrol on HepG2 cell proliferation and migration, and the underlyingmechanism. Methods: Viability of resveratrol (0-200 μmol/L)-treated HepG2 cells wasdetected by CCK-8. Wound healing assay was employed to evaluate cell migration. Theexpression levels of proteins including Bcl-2, Bax, Caspase3, SIRT1, and components of theMAPK pathway were analyzed via Western blot. Results: Resveratrol significantly inhibitedthe migration and proliferation of HepG2 cells at concentrations above 100 μmol/L(P<0.01). The expression of Bax, cleaved Caspase3 and SIRT1 was up-regulate (P<0.05)and Bcl-2, p-JNK、p-p38 MAPK was down-regulate (P<0.05) by resveratrol. Conclusion:Resveratrol suppresses the proliferation and migration of HepG2 cells by activating theSIRT1 signaling pathway and inhibiting the JNK and p38 MAPK pathways.展开更多
Background Abdominal aortic aneurysm(AAA)is a life-threatening vascular disease associated with endothelial cell senescence.Resveratrol(RSV),a natural polyphenol,exerts potent anti-senescent and anti-inflammatory effe...Background Abdominal aortic aneurysm(AAA)is a life-threatening vascular disease associated with endothelial cell senescence.Resveratrol(RSV),a natural polyphenol,exerts potent anti-senescent and anti-inflammatory effects.However,its molecular mechanism in treating AAA remains unclear.Methods An AAA model was established in mice via angiotensin Ⅱ(AngⅡ)infusion[1000 ng/(kg·min)],with a subset receiving RSV treatment[100 mg/(kg·day)by gavage].Aortic diameter was measured,and histopathological changes were assessed by Hematoxylin-Eosin(HE)and Elastica Van Gieson(EVG)staining.Vascular aging was evaluated by senescence-associatedβ-galactosidase(SA-β-gal)activity and pulse wave velocity(PWV).In vitro,human umbilical vein endothelial cells(HUVECs)were treated with AngⅡ(10-6 M)with or without RSV(40μM)and/or the sirtuin 1(SIRT1)inhibitor EX527(10μM).Senescence markers,senescence-associated secretory phenotype(SASP)factor expression[interleukin-1 beta(IL-1β),interleukin-6(IL-6),tumor necrosis factor-alpha(TNF-α)],and SIRT1/p21 pathway proteins were analyzed.Results In vivo,RSV significantly attenuated Ang Ⅱ-induced AAA formation,reducing aortic diameter,preserving elastic fiber integrity,and suppressing vascular senescence and stiffness.In HUVECs,Ang Ⅱ-induced senescence and SASP expression were markedly inhibited by RSV.However,these protective effects were abolished by EX527.Mechanistically,RSV reversed the Ang Ⅱ-induced downregulation of SIRT1 and upregulation of p21,which was also blocked by SIRT1 inhibition.Conclusions RSV effectively prevented experimental AAA formation by alleviating vascular aging and endothelial cell senescence.This protective effect was abrogated by the SIRT1 inhibitor EX527,confirming that RSV mitigated AAA development and vascular senescence through the SIRT1/p21 signaling pathway.These findings highlighted RSV as a promising therapeutic candidate for AAA treatment.展开更多
Pancreatic cancer is a highly aggressive malignancy with a poor prognosis and limited therapeutic options.The tumor microenvironment(TME),including cancer-associated fibroblasts(CAFs),plays a pivotal role in tumor pro...Pancreatic cancer is a highly aggressive malignancy with a poor prognosis and limited therapeutic options.The tumor microenvironment(TME),including cancer-associated fibroblasts(CAFs),plays a pivotal role in tumor progression and therapy resistance.Senescent CAFs,which exhibit a senescence-associated secretory phenotype(SASP),further exacerbate cancer growth through inflammatory cytokine secretion.This editorial highlights a study by Jiang et al,which investigates the potential of resveratrol,a natural polyphenolic compound,in targeting senescent CAFs to inhibit pancreatic cancer progression.The study demonstrates that resveratrol reduces senescent CAFs and downregulates SASP factors,thereby disrupting the pro-tumorigenic activities of these cells.Resveratrol’s ability to modulate the TME,induce apoptosis in pancreatic cancer cells,and inhibit metastasis underscores its potential as an adjunctive therapy.This research offers promising insights into novel strategies for improving therapeutic outcomes in pancreatic cancer by targeting the TME and senescent CAFs.展开更多
Background:Mitochondrial dysfunction plays a critical role in the pathogenesis of Alzheimer’s disease(AD).Resveratrol is a promising compound for the treatment of various neurodegenerative diseases,including AD.Aims:...Background:Mitochondrial dysfunction plays a critical role in the pathogenesis of Alzheimer’s disease(AD).Resveratrol is a promising compound for the treatment of various neurodegenerative diseases,including AD.Aims:To investigate mitochondrial damage and the effects of resveratrol on inflammation,cognitive function,and mitochondrial quality control in APP/PS1 mice.Methods:Comparative analysis of mitochondrial DNA(mtDNA)damage was conducted between 10-month-old APP/PS1 mice and age-matched C57BL/6 mice.Assessments included measurement of amyloid-βlevels,inflammatory markers,swimming distance in the Morris water maze,and gut microbiome composition.Resveratrol’s effects on cytokine expression,mtDNA levels in plasma,and activation of Nuclear factor erythroid 2-related factor 2/Antioxidant response element(Nrf2/ARE)and phosphoinositide 3-kinase/protein kinase B(also known as Akt)/mechanistic target of rapamycin complex 1(PI3K/Akt/mTORC1)signaling pathways were also evaluated.Results:APP/PS1 mice exhibited significantly increased mtDNA damage in the prefrontal cortex,midbrain,and cerebellum,alongside higher amyloid-βlevels and inflammatory markers.Resveratrol treatment led to reduced expression of pro-inflammatory cytokines,a decrease in Proteobacteria levels,and lower cell-free mtDNA in plasma.Partial improvement in long-term spatial memory was observed in APP/PS1 mice following resveratrol treatment,likely due to its anti-inflammatory properties.Activation of the Nrf2/ARE signaling pathway and markers of PI3K/Akt/mTORC1 axis activation were noted,with the latter regulating long-term potentiation.Conclusion:Resveratrol demonstrates potential in mitigating inflammation and improving mitochondrial quality control in APP/PS1 mice,but it does not reduce amyloid-βlevels,highlighting the complexity of AD pathology and the need for further research.展开更多
Ischemic stroke(IS)is a prevalent neurological disorder often resulting in significant disability or mortality.Resveratrol,extracted from Polygonum cuspidatum Sieb.et Zucc.(commonly known as Japanese knotweed),has bee...Ischemic stroke(IS)is a prevalent neurological disorder often resulting in significant disability or mortality.Resveratrol,extracted from Polygonum cuspidatum Sieb.et Zucc.(commonly known as Japanese knotweed),has been recognized for its potent neuroprotective properties.However,the neuroprotective efficacy of its derivative,(E)-4-(3,5-dimethoxystyryl)quinoline(RV02),against ischemic stroke remains inadequately explored.This study aimed to evaluate the protective effects of RV02 on neuronal ischemia-reperfusion injury both in vitro and in vivo.The research utilized an animal model of middle cerebral artery occlusion/reperfusion and SH-SY5Y cells subjected to oxygen-glucose deprivation and reperfusion to simulate ischemic conditions.The findings demonstrate that RV02 attenuates neuronal mitochondrial damage and scavenges reactive oxygen species(ROS)through mitophagy activation.Furthermore,Parkin knockdown was found to abolish RV02's ability to activate mitophagy and neuroprotection in vitro.These results suggest that RV02 shows promise as a neuroprotective agent,with the activation of Parkin-mediated mitophagy potentially serving as the primary mechanism underlying its neuroprotective effects.展开更多
Resveratrol is a kind of polyphenolic compound that widely exists in plants and has extensive physiological pharmacological function and is very useful for human health. For the mechanism of action and function of RV,...Resveratrol is a kind of polyphenolic compound that widely exists in plants and has extensive physiological pharmacological function and is very useful for human health. For the mechanism of action and function of RV, people are doing a variety of groundbreaking researches. Results show that the molecular mechanism of RV is embodied in aspects such as oxidative stress and diseases of neuropathy, anti-oxygenation and pro-oxidant effect and RV target molecule, etc. This article mainly summarized the mechanism of action of resveratrol in these aspects.展开更多
Background: Resveratrol, a plant phenol, affords protection against inflammation and oxidative stress. The objective of this study was to investigate the effects of dietary resveratrol supplementation during pregnancy...Background: Resveratrol, a plant phenol, affords protection against inflammation and oxidative stress. The objective of this study was to investigate the effects of dietary resveratrol supplementation during pregnancy and lactation on the antioxidant status of sows and piglets and on antioxidant gene expression and pathway in placenta.Methods: Forty sows were allotted to 2 dietary treatments 20 d after breeding. Sows were fed a control diet and a control diet with 300 mg/kg resveratrol. Oxidative stress biomarkers and antioxidant enzymes were measured in the placenta, milk, and plasma of sows and piglets. Antioxidant gene expression and protein expression of Kelch-like ECH-associated protein 1-Nuclear factor E2-related factor 2(Keap1-Nrf2), nuclear factor kappa B-p65(NFκB-p65) and sirtuin1(Sirt1) were quantified in the placenta.Results: Dietary resveratrol increased the litter and piglets weaning weights. Antioxidant status in the milk, placenta and plasma of sows and piglets was partially improved by dietary resveratrol. In placenta, Nrf2 protein expression was increased and Keap1 protein expression was decreased by dietary resveratrol. The m RNA expression of antioxidant genes including catalase(CAT), glutathione peroxidase 1(GPX1), GPX4, superoxide dismutase 1(SOD1)and heme oxygenase 1(HO1), and phase 2 detoxification genes, including glutamate-cysteine ligase modifier(GCLM), microsomal glutathione S-transferase 1(MGST1) and UDP glucuronosyltransferase family 1 member A1(UGT1 A1), was increased by dietary resveratrol. Dietary resveratrol also increased Sirt1 and phosphorylated NFκB-p65 protein expression in the placenta. We failed to observe any influences of dietary resveratrol on pro-inflammatory cytokine levels, including those of interleukin 1β(IL-1β), IL-6, IL-8 and tumor necrosis factor α(TNF-α). However, we observed that the m RNA expression of IL-8 in placenta was reduced by maternal resveratrol. In addition, dietary resveratrol showed interactive effects with day of lactation on activities of SOD and CAT and levels of malonaldehyde(MDA) and hydrogen peroxide(H2 O2) in milk.Conclusions: Dietary resveratrol supplementation during pregnancy and lactation improves the antioxidant status of sows and piglets, which is beneficial to the reproductive performance of sows. Dietary resveratrol regulates placental antioxidant gene expression by the Keap1-Nrf2 pathway and Sirt1 in placenta.展开更多
Objective To explore the effects of resveratrol-induced apoptosis and autophagy in T-cell acute lymphoblastic leukemia （T-ALL） cells and potential molecular mechanisms. Methods The anti-proliferation effect of resve...Objective To explore the effects of resveratrol-induced apoptosis and autophagy in T-cell acute lymphoblastic leukemia （T-ALL） cells and potential molecular mechanisms. Methods The anti-proliferation effect of resveratrol-induced, apoptosis and autophagy on T-ALL cells were detected by using MTI- test, immunofluorescence, electronic microscope, and flow cytometry, respectively. Western blotting was performed for detecting changes of apoptosis-associated proteins, cell cycle regulatory proteins and state of activation of Akt, mTOR, p70S6K, 4E-BP1, and p38-MAPK. Results Resveratrol inhibited the proliferation and dose and time-dependent manner. It also induced cyclin-dependent kinase （CDK） inhibitors p21 and induced apoptosis and autophagy in T-ALL cells in a cell cycle arrest at G0/G1 phase via up regulating p27 and down regulating cyclin A and cyclin D1. Western blotting revealed that resveratrol significantly decreased the expression of antiapoptotic proteins （Mcl-1 and Bcl-2） and increased the expression of proapoptotic proteins （Bax, Bim, and Bad）, and induced cleaved-caspase-3 in a time-dependent manner. Significant increase in ratio of LC3-11/LC3-1 and Beclin 1 was also detected. Furthermore, resveratrol induced significant dephosphorylation of Akt, mTOR, p70S6K, and 4E-BP1, but enhanced specific phosphorylation of p38-MAPK which could be blocked by SB203580. When autophagy was suppressed by 3-MA, apoptosis in T-ALL cells induced by resveratrol was enhanced. Conclusion Our findings have suggested that resveratrol induces cell cycle arrest, apoptosis, and autophagy in T-ALL cells through inhibiting Akt/mTOR/p7OS6K/4E-BP1 and activating p38-MAPK signaling pathways. Autophagy might play a role as a self-defense mechanism in T-ALL cells treated by resveratrol. Therefore, the reasonable inhibition of autophagy in T-ALL cells may serve as a promising strategy for resveratrol induced apoptosis and can be used as adjuvant chemotherapy for T-ALL.展开更多
AIM: To determine the therapeutic efficacy of resveratrol on ulcerative colitis (UC) and its underlying mechanisms. METHODS: The mouse UC model was developed using 5% dextran sulfate sodium. Mice were randomly divided...AIM: To determine the therapeutic efficacy of resveratrol on ulcerative colitis (UC) and its underlying mechanisms. METHODS: The mouse UC model was developed using 5% dextran sulfate sodium. Mice were randomly divided into four groups: normal control, UC model group, resveratrol low-dose group (RLD; 50 mg/kg per day), and resveratrol high-dose group (RHD; 100 mg/kg per day). RESULTS: The results showed that RLD regulates Treg/Th17 balance mainly through reducing the number of Th17 cells, whereas RHD regulates Treg/Th17 balance through both downregulating the number of Th17 cells and upregulating the number of Treg cells. Resveratrol can also regulate the level of plasma and intestinal mucosal cytokines including interleukin (IL)-10, transforming growth factor-beta 1, IL-6, and IL-17. The expressions of hypoxia inducible factor (HIF)-1 alpha, mammalian target of rapamycin (mTOR), and signal transducer and activator of transcription 3 were significantly decreased in the intestinal tissues of mice treated with resveratrol. CONCLUSION: The therapeutic efficacy of resveratrol in UC is dose dependent and closely associated with the regulation of Treg/Th17 balance and the HIF-1 alpha/mTOR signaling pathway.展开更多
Gastric cancer(GC) is the fourth most common cancer and the second leading cause of cancer-related mortality in the world. Late diagnosis and classical therapeutic approaches such as surgery, chemotherapy and radiothe...Gastric cancer(GC) is the fourth most common cancer and the second leading cause of cancer-related mortality in the world. Late diagnosis and classical therapeutic approaches such as surgery, chemotherapy and radiotherapy make this disease a still threatening tumor.Genetic asset, environmental stress, dietary habit and infections caused by Helicobacter pylori(H. pylori) arethe major causes concurring to GC initiation. A common mechanism is induction of radicals resulting in gastric mucosal injury. A regular food intake of antioxidant and radical scavenging agents has been proposed to exert protection against tumorigenesis. Resveratrol belongs to the polyphenol flavonoids class of antioxidants produced by a restricted number of plants. Resveratrol exerts bactericidal activity against H. pylori and is a powerful antioxidant, thus acting as a tumor preventive agent.Resveratrol intracellular signaling results in growth arrest and apoptosis, so that it can be directed against tumor progression. Resveratrol therapeutic potential against GC initiation and progression are reviewed here.展开更多
基金supported by the Health Commission of Hubei Province scientific research project(No.WJ2021M143)the Fundamental Research Funds for the Central Universities(No.413000714)+2 种基金the Research Fund of Anhui Institute of translational medicine(No.2023zhyx-C61)the Research Fund Project of Anhui Medical University(No.2022xkj148)Hubei Society of Pathology General Project(No.2025HBAP013).
文摘Epilepsy is a complex neurological disorder aggravated by chronic neuroinflammation largely driven by reactive astrocytes.These cells promote epileptogenesis through persistent cytokine secretion and glial scar formation.Current antiepileptic drugs remain ineffective in targeting these mechanisms due to limited blood-brain barrier(BBB)permeability and poor astrocytic specificity.A transferrin-functionalized biomimetic nanotherapeutic loaded with resveratrol(RN@RTA)was developed to regulate astrocyte-mediated inflammation by activating sirtuin 1(SIRT1)and suppressing the mitogen-activated protein kinase/nuclear factor Kappalight-chain-enhancer of activated B cells(MAPK/NF-κB)axis.Using in vitro BBB models,primary astrocytes,and a pilocarpine-induced chronic epilepsy mouse model,we evaluated the capacity of RN@RTA to cross the BBB,inhibit inflammatory signaling,and reduce seizure activity.Mechanistic assays included immunoprecipitation of NF-κB complexes,cytokine quantification,RNA sequencing,and histopathological assessments of glial and synaptic markers.RN@RTA achieved 82%uptake by hippocampal astrocytes and significantly reduced Il6,Tnf-α,and Nlrp3 expression.SIRT1 activation disrupted the NF-κB p65/p300 complex,leading to transcriptional repression of inflammatory genes and enhancement of autophagy.In vivo,seizure frequency decreased by 67%,synaptic structure was preserved,and astrogliosis was markedly alleviated.The findings demonstrate a dual regulatory mechanism in which RN@RTA suppresses neuroinflammatory signaling and restores neural homeostasis,offering a promising molecularly targeted approach for refractory epilepsy.
文摘The objective of this research was to assess the potential of phosphatidylcholineencapsulated resveratrol as a cosmetic ingredient.The hydrogen peroxide(H_(2)O_(2))and ultraviolet A(UVA)induced human skin fibroblasts(HSF)models of skin damage were established to compare the antioxidant and anti-wrinkle properties between phosphatidylcholine-encapsulated resveratrol and unencapsulated resveratrol.The findings reveal that encapsulating resveratrol with phosphatidylcholine not only enhances skin absorption but also significantly improves its antioxidant capabilities.In the H2O2-induced HSF injury model,phosphatidylcholine-encapsulated resveratrol demonstrates a superior ability to neutralize reactive oxygen species(ROS)generated by H2O2 compared to the resveratrol group.Further analysis indicates that this enhanced functionality is associated with increased enzymatic activities of superoxide dismutase(SOD),glutathione peroxidase(GSH-Px)and catalase(CAT)when treated with phosphatidylcholine-encapsulated resveratrol.Additionally,in UVA-irradiated HSF cells,phosphatidylcholine-encapsulated resveratrol effectively reduces the levels of matrix metalloproteinases-1 and-3(MMP-1 and MMP-3)and increased the contents of CollagenⅠand CollagenⅢ(Col-1 and Col-3),demonstrating significant anti-wrinkle effects.These findings provide critical evaluation criteria and application references for enhancing cosmetic ingredients through phosphatidylcholine encapsulation,thereby advancing skincare formulations.
基金supported by NIH grants, NINDS R21 NS116720 and NINDS/NIA RF1 NS130681 (to RG and WJM)。
文摘The dietary polyphenolic compounds resveratrol and quercetin prevent neurodegenerative diseases in experimental models;however, they reach the brain only in nanomolar concentrations in the glucuronidated and sulfated forms, and not as the aglycone parent form(Pasinetti et al.,2015).
基金supported by the Zhejiang Provincial Science and Technology Department Key Research and Development Plan(No.2020C03046).
文摘Objective Resveratrol(Res)is a promising anticancer drug against hepatocellular carcinoma(HCC),but whether its anti-HCC effects implicate mitophagy remains unclear.Therefore,we aimed to explore the specific role of Res in mitophagy and the related mechanisms during the treatment of HCC.Methods HepG2 cells and tumor-grafted nude mice were used to investigate the effects of low-,middle-and high-dose of Res on HCC progression and mitophagy in vitro and in vivo,respectively.A series of approaches including cell counting kit-8,flow cytometry,wound healing and transwell assays were used to evaluate tumor cell functions.Transmission electron microscopy,immunofluorescence and Western blotting analysis were used to assess mitophagy.Mitochondrial oxygen consumption rate,reactive oxygen species and membrane potential were used to reflect mitochondrial function.After disrupting the expression of metastasis-associated lung adenocarcinoma transcript 1(MALAT1),miR-143-3p,and ribonucleoside reductase M2(RRM2),the effects of the MALAT1/miR-143-3p/RRM2 axis on cell function and mitophagy under Res treatment were explored in vitro.Additionally,dual-luciferase reporter and chromatin immunoprecipitation were used to confirm interactions between target genes.Results Res significantly inhibited the proliferation and promoted apoptosis of HCC cells in vitro,while significantly suppressing tumor growth in a dose-dependent manner and inducing mitophagy and mitochondrial dysfunction in vivo.Interestingly,MALAT1 was highly expressed in HCC cells and its knockdown upregulated miR-143-3p expression in HCC cells,which subsequently inhibited RRM2 expression.Furthermore,in nude mice grafted with HCC tumors and treated with Res,the expression of MALAT1,miR-143-3p and RRM2 were altered significantly.In vitro data further supported the targeted binding relationships between MALAT1 and miR-143-3p and between miR-143-3p and RRM2.Therefore,a series of cell-based experiments were carried out to study the mechanism of the MALAT1/miR-143-3p/RRM2 axis involved in mitophagy and HCC;these experiments revealed that MALAT1 knockdown,miR-143-3p mimic and RRM silencing potentiated the antitumor effects of Res and its activation of mitophagy.Conclusion Res facilitated mitophagy in HCC and exerted anti-cancer effects by targeting the MALAT1/miR-143-3p/RRM2 axis.
文摘Aim To synthesize a new prodrug, resveratrol trinicotinate. Methods Inpresence of lithium and a catalytic amount of naphthalene, the reaction of p-methoxybenzyltrimethylsilyl ether and 3,5-dimethoxylbenzaldehyde gave resveratrol after a series of translation.Resveratrol trinicotinate was obtained by the reaction of resveratrol and nicotinoyl chloridehydrochloride. Results A mutual prodrug resveratrol trinicotinate was designed and synthesized.Conclusion A novel method for synthesis of resveratrol and resveratrol trinicotinate has beenafforded. The E-isomer is selectivily obtained by dehydration of the compound 2 with KHSO_4 .
文摘There is still no effective treatment for pancreatic cancer,one of the deadliest malignancies among the gastrointestinal diseases.Jiang et al demonstrated the presence of senescent cancer-associated fibroblasts(CAFs)in pancreatic cancer tissues,supporting the use of CAFs as potential anti-cancer targets.The study indicated that a natural plant-derived compound resveratrol can reverse senescent CAF phenotype and decrease the growth,migration,and invasiveness of pancreatic cancer cells.Notably,the study indicated that resveratrol might be involved in regulating epithelial-to-mesenchymal transition in the tumor microenvironment.This editorial shares insights on the future investigation of resveratrol signaling in cancer cells and the tumor microenvironment,and discusses resveratrol-based treatment perspectives.
文摘Emerging evidence highlights the potential of bioactive compounds,particularly polyphenols,as adjunctive therapeutic agents in the treatment of pancreatic cancer(PC),one of the most aggressive malignancies.This review focuses on epigallocatechin gallate(EGCG)and resveratrol due to their extensively documented anticancer activity,favorable safety profiles,and their unique ability to modulate multiple signaling pathways relevant to pan-creatic tumorigenesis.Among polyphenols,these two have shown superior anti-cancer activity,epigenetic regulatory effects,and synergy with standard chemotherapies in preclinical pancreatic cancer models.Resveratrol exhibits anti-proliferative effects by modulating key signaling pathways,including phosphatidylinositol 3 kinase(PI3K)/protein kinase B(Akt),nuclear factor kappa-B(NF-κB),and tumor protein 53(p53).EGCG exerts anti-cancer activity by targeting multiple cellular processes,such as oxidative stress reduction,and suppression of inflammatory mediators like Interleukin-6(IL-6)and Tumor Necrosis Factor-α(TNF-α).Both EGCG and resveratrol exert anti-pancreatic cancer effects partly through direct interactions with cell surface receptors and modulation of intracellular cascades.EGCG targets the 67 kDa laminin receptor(67LR),which is overexpressed in pancreatic cancer cells,triggering apoptosis,cyclic guanosine monophosphate(cGMP)production and activation of the PKCδ/acid sphingomyelinase(ASM)cascade.Resveratrol inhibits insulin-like growth factor-1 receptor(IGF-1R)activation of the PI3K/Akt and Wnt signaling pathways,while concurrently activating tumor suppressor p53.These interactions suppress proliferation,promote apoptosis,and reduce epithelial-mesenchymal transition(EMT),thereby limiting tumor progression.Both polyphenols enhance chemosensitivity and reduce resistance to conventional therapies,including gemcitabine,by modulating drug transporters and apoptotic pathways.Furthermore,their epigenetic influence,particularly via DNA methylation and histone modification,suggests a broader role in pancreatic cancer prevention.Understanding the roles and mechanisms of resveratrol and EGCG in pancreatic cancer provides valuable insights into novel treatment strategies.The integration of polyphenols into conventional therapeutic approaches may offer new hope for improving patient outcomes.
基金supported by Natural Science Foundation of Nanjing University of Chinese Medicine(XZR2023010)Traditional Chinese Medicine Science and Technology Project of Jiangsu Province(QN202212)Guidance Program of Jiangsu Commission of Health(Z2020046).
文摘Background: Resveratrol is a widely recognized anti-inflammatory and antioxidant agent,and it has been suggested to possess anti-tumor effects. But the effect of resveratrol onhepatocellular carcinoma and its molecular mechanisms are unknown. This study confirmedthe effects of resveratrol on HepG2 cell proliferation and migration, and the underlyingmechanism. Methods: Viability of resveratrol (0-200 μmol/L)-treated HepG2 cells wasdetected by CCK-8. Wound healing assay was employed to evaluate cell migration. Theexpression levels of proteins including Bcl-2, Bax, Caspase3, SIRT1, and components of theMAPK pathway were analyzed via Western blot. Results: Resveratrol significantly inhibitedthe migration and proliferation of HepG2 cells at concentrations above 100 μmol/L(P<0.01). The expression of Bax, cleaved Caspase3 and SIRT1 was up-regulate (P<0.05)and Bcl-2, p-JNK、p-p38 MAPK was down-regulate (P<0.05) by resveratrol. Conclusion:Resveratrol suppresses the proliferation and migration of HepG2 cells by activating theSIRT1 signaling pathway and inhibiting the JNK and p38 MAPK pathways.
基金supported by the grant from the Fujian Province Natural Science Foundation(No.2024J01608)。
文摘Background Abdominal aortic aneurysm(AAA)is a life-threatening vascular disease associated with endothelial cell senescence.Resveratrol(RSV),a natural polyphenol,exerts potent anti-senescent and anti-inflammatory effects.However,its molecular mechanism in treating AAA remains unclear.Methods An AAA model was established in mice via angiotensin Ⅱ(AngⅡ)infusion[1000 ng/(kg·min)],with a subset receiving RSV treatment[100 mg/(kg·day)by gavage].Aortic diameter was measured,and histopathological changes were assessed by Hematoxylin-Eosin(HE)and Elastica Van Gieson(EVG)staining.Vascular aging was evaluated by senescence-associatedβ-galactosidase(SA-β-gal)activity and pulse wave velocity(PWV).In vitro,human umbilical vein endothelial cells(HUVECs)were treated with AngⅡ(10-6 M)with or without RSV(40μM)and/or the sirtuin 1(SIRT1)inhibitor EX527(10μM).Senescence markers,senescence-associated secretory phenotype(SASP)factor expression[interleukin-1 beta(IL-1β),interleukin-6(IL-6),tumor necrosis factor-alpha(TNF-α)],and SIRT1/p21 pathway proteins were analyzed.Results In vivo,RSV significantly attenuated Ang Ⅱ-induced AAA formation,reducing aortic diameter,preserving elastic fiber integrity,and suppressing vascular senescence and stiffness.In HUVECs,Ang Ⅱ-induced senescence and SASP expression were markedly inhibited by RSV.However,these protective effects were abolished by EX527.Mechanistically,RSV reversed the Ang Ⅱ-induced downregulation of SIRT1 and upregulation of p21,which was also blocked by SIRT1 inhibition.Conclusions RSV effectively prevented experimental AAA formation by alleviating vascular aging and endothelial cell senescence.This protective effect was abrogated by the SIRT1 inhibitor EX527,confirming that RSV mitigated AAA development and vascular senescence through the SIRT1/p21 signaling pathway.These findings highlighted RSV as a promising therapeutic candidate for AAA treatment.
基金Supported by National Natural Science Foundation of China,No.82304151.
文摘Pancreatic cancer is a highly aggressive malignancy with a poor prognosis and limited therapeutic options.The tumor microenvironment(TME),including cancer-associated fibroblasts(CAFs),plays a pivotal role in tumor progression and therapy resistance.Senescent CAFs,which exhibit a senescence-associated secretory phenotype(SASP),further exacerbate cancer growth through inflammatory cytokine secretion.This editorial highlights a study by Jiang et al,which investigates the potential of resveratrol,a natural polyphenolic compound,in targeting senescent CAFs to inhibit pancreatic cancer progression.The study demonstrates that resveratrol reduces senescent CAFs and downregulates SASP factors,thereby disrupting the pro-tumorigenic activities of these cells.Resveratrol’s ability to modulate the TME,induce apoptosis in pancreatic cancer cells,and inhibit metastasis underscores its potential as an adjunctive therapy.This research offers promising insights into novel strategies for improving therapeutic outcomes in pancreatic cancer by targeting the TME and senescent CAFs.
基金supported by the Russian science foundation(grant#22-74-00115 to A.P.G.).
文摘Background:Mitochondrial dysfunction plays a critical role in the pathogenesis of Alzheimer’s disease(AD).Resveratrol is a promising compound for the treatment of various neurodegenerative diseases,including AD.Aims:To investigate mitochondrial damage and the effects of resveratrol on inflammation,cognitive function,and mitochondrial quality control in APP/PS1 mice.Methods:Comparative analysis of mitochondrial DNA(mtDNA)damage was conducted between 10-month-old APP/PS1 mice and age-matched C57BL/6 mice.Assessments included measurement of amyloid-βlevels,inflammatory markers,swimming distance in the Morris water maze,and gut microbiome composition.Resveratrol’s effects on cytokine expression,mtDNA levels in plasma,and activation of Nuclear factor erythroid 2-related factor 2/Antioxidant response element(Nrf2/ARE)and phosphoinositide 3-kinase/protein kinase B(also known as Akt)/mechanistic target of rapamycin complex 1(PI3K/Akt/mTORC1)signaling pathways were also evaluated.Results:APP/PS1 mice exhibited significantly increased mtDNA damage in the prefrontal cortex,midbrain,and cerebellum,alongside higher amyloid-βlevels and inflammatory markers.Resveratrol treatment led to reduced expression of pro-inflammatory cytokines,a decrease in Proteobacteria levels,and lower cell-free mtDNA in plasma.Partial improvement in long-term spatial memory was observed in APP/PS1 mice following resveratrol treatment,likely due to its anti-inflammatory properties.Activation of the Nrf2/ARE signaling pathway and markers of PI3K/Akt/mTORC1 axis activation were noted,with the latter regulating long-term potentiation.Conclusion:Resveratrol demonstrates potential in mitigating inflammation and improving mitochondrial quality control in APP/PS1 mice,but it does not reduce amyloid-βlevels,highlighting the complexity of AD pathology and the need for further research.
基金supported by the National Natural ScienceFoundation of China (No.82174076)the Construction Project of Liaoning Provincial Key Laboratory,China (No.2022JH13/10200026)+2 种基金the Fundamental Research Funds for the Central Universities (No.N2220002)the 111 Project (No.B16009)the Research Project of Educational Commission of Liaoning Province (No.LJ212410164003)。
文摘Ischemic stroke(IS)is a prevalent neurological disorder often resulting in significant disability or mortality.Resveratrol,extracted from Polygonum cuspidatum Sieb.et Zucc.(commonly known as Japanese knotweed),has been recognized for its potent neuroprotective properties.However,the neuroprotective efficacy of its derivative,(E)-4-(3,5-dimethoxystyryl)quinoline(RV02),against ischemic stroke remains inadequately explored.This study aimed to evaluate the protective effects of RV02 on neuronal ischemia-reperfusion injury both in vitro and in vivo.The research utilized an animal model of middle cerebral artery occlusion/reperfusion and SH-SY5Y cells subjected to oxygen-glucose deprivation and reperfusion to simulate ischemic conditions.The findings demonstrate that RV02 attenuates neuronal mitochondrial damage and scavenges reactive oxygen species(ROS)through mitophagy activation.Furthermore,Parkin knockdown was found to abolish RV02's ability to activate mitophagy and neuroprotection in vitro.These results suggest that RV02 shows promise as a neuroprotective agent,with the activation of Parkin-mediated mitophagy potentially serving as the primary mechanism underlying its neuroprotective effects.
文摘Resveratrol is a kind of polyphenolic compound that widely exists in plants and has extensive physiological pharmacological function and is very useful for human health. For the mechanism of action and function of RV, people are doing a variety of groundbreaking researches. Results show that the molecular mechanism of RV is embodied in aspects such as oxidative stress and diseases of neuropathy, anti-oxygenation and pro-oxidant effect and RV target molecule, etc. This article mainly summarized the mechanism of action of resveratrol in these aspects.
基金supported by the National Key Research and Development Plan of China(2016YFD0501207)the China Agriculture Research System(CARS-36)the National Basic Research Program(2012CB124703)
文摘Background: Resveratrol, a plant phenol, affords protection against inflammation and oxidative stress. The objective of this study was to investigate the effects of dietary resveratrol supplementation during pregnancy and lactation on the antioxidant status of sows and piglets and on antioxidant gene expression and pathway in placenta.Methods: Forty sows were allotted to 2 dietary treatments 20 d after breeding. Sows were fed a control diet and a control diet with 300 mg/kg resveratrol. Oxidative stress biomarkers and antioxidant enzymes were measured in the placenta, milk, and plasma of sows and piglets. Antioxidant gene expression and protein expression of Kelch-like ECH-associated protein 1-Nuclear factor E2-related factor 2(Keap1-Nrf2), nuclear factor kappa B-p65(NFκB-p65) and sirtuin1(Sirt1) were quantified in the placenta.Results: Dietary resveratrol increased the litter and piglets weaning weights. Antioxidant status in the milk, placenta and plasma of sows and piglets was partially improved by dietary resveratrol. In placenta, Nrf2 protein expression was increased and Keap1 protein expression was decreased by dietary resveratrol. The m RNA expression of antioxidant genes including catalase(CAT), glutathione peroxidase 1(GPX1), GPX4, superoxide dismutase 1(SOD1)and heme oxygenase 1(HO1), and phase 2 detoxification genes, including glutamate-cysteine ligase modifier(GCLM), microsomal glutathione S-transferase 1(MGST1) and UDP glucuronosyltransferase family 1 member A1(UGT1 A1), was increased by dietary resveratrol. Dietary resveratrol also increased Sirt1 and phosphorylated NFκB-p65 protein expression in the placenta. We failed to observe any influences of dietary resveratrol on pro-inflammatory cytokine levels, including those of interleukin 1β(IL-1β), IL-6, IL-8 and tumor necrosis factor α(TNF-α). However, we observed that the m RNA expression of IL-8 in placenta was reduced by maternal resveratrol. In addition, dietary resveratrol showed interactive effects with day of lactation on activities of SOD and CAT and levels of malonaldehyde(MDA) and hydrogen peroxide(H2 O2) in milk.Conclusions: Dietary resveratrol supplementation during pregnancy and lactation improves the antioxidant status of sows and piglets, which is beneficial to the reproductive performance of sows. Dietary resveratrol regulates placental antioxidant gene expression by the Keap1-Nrf2 pathway and Sirt1 in placenta.
基金supported by grants from the Department of Science and Technology of Sichuan Province,China (No.2008JY0029-1 and No.07FG002-024)research funds from the Program for Changjiang Scholars and Innovative-Research Team in University (No.IRT0935)
文摘Objective To explore the effects of resveratrol-induced apoptosis and autophagy in T-cell acute lymphoblastic leukemia （T-ALL） cells and potential molecular mechanisms. Methods The anti-proliferation effect of resveratrol-induced, apoptosis and autophagy on T-ALL cells were detected by using MTI- test, immunofluorescence, electronic microscope, and flow cytometry, respectively. Western blotting was performed for detecting changes of apoptosis-associated proteins, cell cycle regulatory proteins and state of activation of Akt, mTOR, p70S6K, 4E-BP1, and p38-MAPK. Results Resveratrol inhibited the proliferation and dose and time-dependent manner. It also induced cyclin-dependent kinase （CDK） inhibitors p21 and induced apoptosis and autophagy in T-ALL cells in a cell cycle arrest at G0/G1 phase via up regulating p27 and down regulating cyclin A and cyclin D1. Western blotting revealed that resveratrol significantly decreased the expression of antiapoptotic proteins （Mcl-1 and Bcl-2） and increased the expression of proapoptotic proteins （Bax, Bim, and Bad）, and induced cleaved-caspase-3 in a time-dependent manner. Significant increase in ratio of LC3-11/LC3-1 and Beclin 1 was also detected. Furthermore, resveratrol induced significant dephosphorylation of Akt, mTOR, p70S6K, and 4E-BP1, but enhanced specific phosphorylation of p38-MAPK which could be blocked by SB203580. When autophagy was suppressed by 3-MA, apoptosis in T-ALL cells induced by resveratrol was enhanced. Conclusion Our findings have suggested that resveratrol induces cell cycle arrest, apoptosis, and autophagy in T-ALL cells through inhibiting Akt/mTOR/p7OS6K/4E-BP1 and activating p38-MAPK signaling pathways. Autophagy might play a role as a self-defense mechanism in T-ALL cells treated by resveratrol. Therefore, the reasonable inhibition of autophagy in T-ALL cells may serve as a promising strategy for resveratrol induced apoptosis and can be used as adjuvant chemotherapy for T-ALL.
基金Supported by Outstanding Doctoral Thesis Support Project of Guangdong Province,No.85514045the Technical Research and Development Project of Shenzhen,No.JCYJ20130402092657774the Medical Research Foundation of Guangdong Province,No.B2013347
文摘AIM: To determine the therapeutic efficacy of resveratrol on ulcerative colitis (UC) and its underlying mechanisms. METHODS: The mouse UC model was developed using 5% dextran sulfate sodium. Mice were randomly divided into four groups: normal control, UC model group, resveratrol low-dose group (RLD; 50 mg/kg per day), and resveratrol high-dose group (RHD; 100 mg/kg per day). RESULTS: The results showed that RLD regulates Treg/Th17 balance mainly through reducing the number of Th17 cells, whereas RHD regulates Treg/Th17 balance through both downregulating the number of Th17 cells and upregulating the number of Treg cells. Resveratrol can also regulate the level of plasma and intestinal mucosal cytokines including interleukin (IL)-10, transforming growth factor-beta 1, IL-6, and IL-17. The expressions of hypoxia inducible factor (HIF)-1 alpha, mammalian target of rapamycin (mTOR), and signal transducer and activator of transcription 3 were significantly decreased in the intestinal tissues of mice treated with resveratrol. CONCLUSION: The therapeutic efficacy of resveratrol in UC is dose dependent and closely associated with the regulation of Treg/Th17 balance and the HIF-1 alpha/mTOR signaling pathway.
文摘Gastric cancer(GC) is the fourth most common cancer and the second leading cause of cancer-related mortality in the world. Late diagnosis and classical therapeutic approaches such as surgery, chemotherapy and radiotherapy make this disease a still threatening tumor.Genetic asset, environmental stress, dietary habit and infections caused by Helicobacter pylori(H. pylori) arethe major causes concurring to GC initiation. A common mechanism is induction of radicals resulting in gastric mucosal injury. A regular food intake of antioxidant and radical scavenging agents has been proposed to exert protection against tumorigenesis. Resveratrol belongs to the polyphenol flavonoids class of antioxidants produced by a restricted number of plants. Resveratrol exerts bactericidal activity against H. pylori and is a powerful antioxidant, thus acting as a tumor preventive agent.Resveratrol intracellular signaling results in growth arrest and apoptosis, so that it can be directed against tumor progression. Resveratrol therapeutic potential against GC initiation and progression are reviewed here.
