AIM To investigate the protective effects of polydatin (PD) against injury to primarily cultured rat hepatocytes induced by CCl 4. METHODS Rat hepatocytes were separated by methods of liver infusion in vivo and cu...AIM To investigate the protective effects of polydatin (PD) against injury to primarily cultured rat hepatocytes induced by CCl 4. METHODS Rat hepatocytes were separated by methods of liver infusion in vivo and cultured medium (7 5×10 5 cells/mL). Two mL or 0 2mL was added into 24 well or 96 well plates respectively. Twenty four hours after cell preculture, PD at concentrations of 10 -7 mol/L-10 -4 mol/L was added into each plate. At the same time injury to hepatocytes was induced by adding 10mmol/L CCl 4. Then, 0 1mL or 1mL culture solution was removed from the 96 well or 24 well plates at 6h , 12h , 24h and 48h after CCl 14 intoxication respectively for the determination of GPT, GSH and MDA. At 48h , the survivability of rat hepatocytes was assayed by the MTT colormetric method. RESULTS After CCl 4 challenge, the release of GPT and the formation of MDA in rat hepatocytes markedly increased and maintained at a high level in 48h , whereas PD with different concentrations could markedly inhibit this elevation with 10 -5 mol/L PD having the strongest effects and inhibiting rate was over 50%. PD could also improve the decreased content of GSH caused by CCl 4 in accordance with the doses used. CCl 4 evidently decreased the hepatocyte survivability from 91 0%±7 9% to 35 4%±3 8%. On the other hand, PD at 10 -7 mol/L-10 -4 mol/L could reverse this change and improve the cell survival rates to 56 1%±5 2%, 65 8%±5 0%, 88 7%±6 8% and 75 2%±7 3%, respectively. CONCLUSION PD at 10 -7 mol/L-10 -4 mol/L could protect primarily cultured rat hepatocytes against CCl 4 induced injury.展开更多
Polydatin is thought to protect mitochondria in different cell types in various diseases.Mitochondrial dysfunction is a major contributing factor in secondary brain injury resulting from traumatic brain injury.To inve...Polydatin is thought to protect mitochondria in different cell types in various diseases.Mitochondrial dysfunction is a major contributing factor in secondary brain injury resulting from traumatic brain injury.To investigate the protective effect of polydatin after traumatic brain injury,a rat brain injury model of lateral fluid percussion was established to mimic traumatic brain injury insults.Rat models were intraperitoneally injected with polydatin(30 mg/kg)or the SIRT1 activator SRT1720(20 mg/kg,as a positive control to polydatin).At 6 hours post-traumatic brain injury insults,western blot assay was used to detect the expression of SIRT1,endoplasmic reticulum stress related proteins and p38 phosphorylation in cerebral cortex on the injured side.Flow cytometry was used to analyze neuronal mitochondrial superoxide,mitochondrial membrane potential and mitochondrial permeability transition pore opened.Ultrastructural damage in neuronal mitochondria was measured by transmission electron microscopy.Our results showed that after treatment with polydatin,release of reactive oxygen species in neuronal mitochondria was markedly reduced;swelling of mitochondria was alleviated;mitochondrial membrane potential was maintained;mitochondrial permeability transition pore opened.Also endoplasmic reticulum stress related proteins were inhibited,including the activation of p-PERK,spliced XBP-1 and cleaved ATF6.SIRT1 expression and activity were increased;p38 phosphorylation and cleaved caspase-9/3 activation were inhibited.Neurological scores of treated rats were increased and the mortality was reduced compared with the rats only subjected to traumatic brain injury.These results indicated that polydatin protectrd rats from the consequences of traumatic brain injury and exerted a protective effect on neuronal mitochondria.The mechanisms may be linked to increased SIRT1 expression and activity,which inhibits the p38 phosphorylation-mediated mitochondrial apoptotic pathway.This study was approved by the Animal Care and Use Committee of the Southern Medical University,China(approval number:L2016113)on January 1,2016.展开更多
AIM: To investigate the effect of polydatin (PD), a resveratrol glucoside, on mast cell degranulation and antiallergic activity. METHODS: After the rats were orally sensitized with ovalbumin (OVA) for 48 d and underwe...AIM: To investigate the effect of polydatin (PD), a resveratrol glucoside, on mast cell degranulation and antiallergic activity. METHODS: After the rats were orally sensitized with ovalbumin (OVA) for 48 d and underwent PD treatment for 4 d, all the rats were stimulated by 100 mg/mL OVA for24 h and then sacrificed for the following experiments. The small intestines from all the groups were prepared for morphology examination by hematoxylin and eosin staining. We also used a smooth muscle organ bath to evaluate the motility of the small intestines. The OVA-specific immunoglobulin E (IgE) production and interleu-kin-4 (IL-4) levels in serum or supernatant of intestinal mucosa homogenates were analyzed by enzyme-linked immunosorbent assay (ELISA). Using toluidine blue stain, the activation and degranulation of isolated rat peritoneal mast cells (RPMCs) were analyzed. Release of histamine from RPMCs was measured by ELISA, and regulation of PD on intracellular Ca 2+ mobilization was investigated by probing intracellular Ca 2+ with fluo-4 fluo-rescent dye, with the signal recorded and analyzed. RESULTS: We found that intragastric treatment with PD significantly reduced loss of mucosal barrier integrity in the small intestine. However, OVA-sensitization caused significant hyperactivity in the small intestine of allergic rats, which was attenuated by PD administration by 42% (1.26 ± 0.13 g vs OVA 2.18 ± 0.21 g, P < 0.01). PD therapy also inhibited IgE production (3.95 ± 0.53 ng/mL vs OVA 4.53 ± 0.52 ng/mL, P < 0.05) by suppressing the secretion of Th2-type cytokine, IL-4, by 34% (38.58 ± 4.41 pg/mLvs OVA 58.15 ± 6.24 pg/mL, P < 0.01). The ratio of degranulated mast cells, as indicated by vehicles (at least five) around the cells, dramatically increased in the OVA group by 5.5 fold (63.50% ± 15.51% vs phosphate-buffered saline 11.15% ± 8.26%, P < 0.001) and fell by 65% after PD treatment (21.95% ± 4.37% vs OVA 63.50% ± 15.51%, P < 0.001). PD mediated attenuation of mast cell degranulation was further confirmed by decreased histamine levels in both serum (5.98 ± 0.17 vs OVA 6.67 ± 0.12, P < 0.05) and intestinal mucosa homogenates (5.83 ± 0.91 vs OVA 7.35 ± 0.97, P < 0.05). Furthermore, we demonstrated that administration with PD significantly decreased mast cell degranulation due to reduced Ca 2+ influx through store-operated calcium channels (SOCs) (2.35 ± 0.39vs OVA 3.51 ± 0.38,P < 0.01).CONCLUSION: Taken together, our data indicate that PD stabilizes mast cells by suppressing intracellular Ca 2+ mobilization, mainly through inhibiting Ca 2+ entry via SOCs, thus exerting a protective role against OVA-sensitized food allergy.展开更多
Background:Polydatin,a glucoside of resveratrol,has shown protective effects against various diseases.However,little is known about its effect on hepatic ischemia-reperfusion(I/R)injury.This study aimed to elucidate w...Background:Polydatin,a glucoside of resveratrol,has shown protective effects against various diseases.However,little is known about its effect on hepatic ischemia-reperfusion(I/R)injury.This study aimed to elucidate whether polydatin protects liver against I/R-induced injury and to explore the underlying mechanism.Methods:After gavage feeding polydatin once daily for a week,mice underwent a partial hepatic I/R procedure.Serum alanine aminotransferase(ALT)/aspartate aminotransferase(AST),hematoxylin-eosin(H&E)and TdT-mediated dUTP nick-end labeling(TUNEL)staining were used to evaluate liver injury.The severity related to the inflammatory response and reactive oxygen species(ROS)production was also investigated.Furthermore,immunofluorescence and Western blotting were used to detect macrophage polarization and the NF-κB signaling pathway in macrophages.Results:Compared with the I/R group,polydatin pretreatment significantly attenuated I/R-induced liver damage and apoptosis.The oxidative stress marker(dihydroethidium fluorescence,malondialdehyde,superoxide dismutase and glutathione peroxidase)and I/R related inflammatory cytokines(interleukin1β,interleukin-10 and tumor necrosis factor-α)were significantly suppressed after polydatin treatment.In addition,the result of immunofluorescence indicated that polydatin reduced the polarization of macrophages toward M1 macrophages both in vivo and in vitro.Western blotting showed that polydatin inhibited the pro-inflammatory function of RAW264.7 via down-regulating the NF-κB signaling pathway.Conclusions:Polydatin protects the liver from I/R injury by remodeling macrophage polarization via NFκB signaling.展开更多
To investigate the effects of polydatin on the proliferation,migration,and invasion of ovarian cancer,the change of proliferative ability,migration ability,and invasive ability of human ovarian cancer cell OVCAR-3,A27...To investigate the effects of polydatin on the proliferation,migration,and invasion of ovarian cancer,the change of proliferative ability,migration ability,and invasive ability of human ovarian cancer cell OVCAR-3,A2780,and HO-8910 was detected by using polydatin and up-regulating PI3K.The anticancer activity and mechanism of polydatin in ovarian cancer were analyzed.Polydatin could effectively inhibit the proliferation,migration,and invasion of OVCAR-3,A2780,and HO-8910,and inhibit the expression of PI3K protein.After the expression level of PI3K protein was up-regulated,the inhibitory effect of polydatin on the proliferative ability,migration ability,and invasive ability of OVCAR-3,A2780,and HO-8910 significantly decreased,suggesting that PI3K was the target of polydatin.Therefore,we concluded that polydatin could inhibit the proliferation,migration,and invasion of ovarian cancer cells by inhibiting the expression of PI3K protein,which provides an experimental basis for polydatin in the treatment of ovarian cancer.展开更多
Objective A method of TLC-fluorescence spectrophotometry was established to assay the content of polydatin in polygonum cuspidatum sieb. et zucc. Methods: Polydatin was extracted by methanol and separated with chloro...Objective A method of TLC-fluorescence spectrophotometry was established to assay the content of polydatin in polygonum cuspidatum sieb. et zucc. Methods: Polydatin was extracted by methanol and separated with chloroform-acetone-formic acid-water (4∶4∶0.5∶0.2) by thin layer chromatography. The excitation wavelength and emission wavelength were 284 nm and 384 nm, respectively. Results The linear regression equation of the calibration graph was y=7.02179x+4.5143, a linear regression correlative coefficient r=0.9936. Conclusion This method was proved simple, stable and sensitive. It can be used in quality control of herbs.展开更多
[Objectives]To establish a UPLC-UV method for the determination of polydatin in the serum of Wistar rats.[Methods]Acquity UPLC BEH shield RP18 column(1.7μm,2.1 mm×100 mm,Waters Corporation,USA)was used as the an...[Objectives]To establish a UPLC-UV method for the determination of polydatin in the serum of Wistar rats.[Methods]Acquity UPLC BEH shield RP18 column(1.7μm,2.1 mm×100 mm,Waters Corporation,USA)was used as the analytical column,acetonitrile-water(55∶45)was used as the mobile phase,the flow rate was 0.5 mL/min,and the column temperature was 30℃and the detection wavelength was 306 nm.[Results]The linear range of the established serum sample analysis method was 1.0-20.0μg/mL,and the correlation coefficient was r=0.9994;the intraday and interday RSD of Wistar rat serum was less than 3.0%,and the accuracy was higher than 90%.[Conclusions]This method is sensitive,accurate,and rapid.It is suitable for monitoring the concentration of polydatin in serum after intragastric administration,and can also be used for pharmacokinetics and bioavailability studies.展开更多
Rheumatological diseases encompass a wide range of conditions primarily affecting the musculoskeletal system.They represent a significant burden on modern society,affecting millions of people worldwide.These chronic a...Rheumatological diseases encompass a wide range of conditions primarily affecting the musculoskeletal system.They represent a significant burden on modern society,affecting millions of people worldwide.These chronic and debilitating conditions require long-term management and a multidisciplinary approach that combines pharmacological interventions with lifestyle modifications for optimal patient outcomes.In this context,diet is emerging as a crucial support in managing rheumatological diseases.Certain dietary patterns and specific nu-trients can play a significant role in reducing inflammation,alleviating symptoms,and potentially slowing disease progression.Bioactive compounds,which are found in many plant-based foods and are abundant in the Mediterranean diet,are increasingly being recognized as valuable supports to traditional treatments in arthritis.Among them,polydatin has shown potent antioxidant and anti-inflammatory properties.This review aims to comprehensively examine the therapeutic potential of polydatin in various rheumato-logical diseases,including rheumatoid arthritis,osteoarthritis,crystal-induced arthritis,spondyloarthritis,and systemic lupus erythematosus.Articles included have been identified using keyword-based searches in multiple scientific databases,including PubMed and Scopus.The review highlights polydatin's multi-targeted mechanisms,including antioxidant activity,modulation of inflammatory pathways,regulation of apoptosis and autophagy,and direct interactions with molecular targets like sirtuin 1 and chemokine receptor type 1.Although clinical studies specifically investigating polydatin in rheumatological conditions are scarce,the translational potential of this compound is supported by randomized controlled trials involving other human inflammatory and pain-related disorders.Polydatin's favorable phar-macokinetic profile,enhanced bioavailability,and diverse biological actions position it as a promising natural compound for managing rheumatological diseases.展开更多
This study investigated the antiepileptic effects of polydatin(PD)and its potential mechanisms.Racine scoring and EEG were used to assess seizure severity in a PTZ-induced mouse epilepsy model.The results demonstrated...This study investigated the antiepileptic effects of polydatin(PD)and its potential mechanisms.Racine scoring and EEG were used to assess seizure severity in a PTZ-induced mouse epilepsy model.The results demonstrated that PD significantly reduced the intensity of seizures.Behavioral tests revealed that PD improved learning,memory,and motor coordination.Histological analysis using HE and Nissl staining showed that PD alleviated hippocampal neuronal damage.TUNEL staining further confirmed that PD effectively prevented neuronal apoptosis.Network pharmacology predicted SIRT1 as a potential target of PD,and GO and KEGG pathway enrichment analyses indicated that PD regulated mitochondrial function.Therefore,PD may reduce neuronal damage by protecting mitochondrial function through SIRT1.This process was tested both in vitro and in vivo.In a Mg^(2+)-free neuronal excitability model,CCK-8,LDH,and Hoechst staining results demonstrated that PD significantly increased cell survival and reduced apoptosis.Reduced mitosox staining,along with increased activity of Complexes IV and V and ATP production,indicated that PD mitigated mitochondrial function.Gene expression studies revealed that PD activated the SIRT1-PGC-1αsignaling pathway via AMPK.In conclusion,PD exerted neuroprotective effects by regulating mitochondrial function,suggesting a potential therapeutic target for epilepsy.展开更多
The NLRP3 inflammasome plays a critical role in various inflammatory conditions.However,despite extensive research in targeted drug development for NLRP3,including MCC950,clinical success remains elusive.Here,we disco...The NLRP3 inflammasome plays a critical role in various inflammatory conditions.However,despite extensive research in targeted drug development for NLRP3,including MCC950,clinical success remains elusive.Here,we discovered that the activated NLRP3 inflammasome complex(disc-NLRP3)and the activating mutation L351P exhibited resistance to MCC950.Through investigations using the small-molecule compound polydatin,HSP90αwas found to stabilize both the resting(cage-NLRP3)and activated state(disc-NLRP3)of NLRP3 complexes,sustaining its activation.Our mechanistic studies revealed that polydatin specifically targets HSP90α,binding to it directly and subsequently interfering with the HSP90α-NLRP3 interaction.This disruption leads to the dissipation of cage-NLRP3,disc-NLRP3 complexes and NLRP3 L351P.Importantly,genetic and pharmacological inactivation of HSP90αeffectively reduced NLRP3 inflammasome activation and alleviated cerulein-induced acute pancreatitis.These therapeutic effects highlight the clinical potential of HSP90αinhibition.Our findings demonstrate that HSP90αis crucial for the stability of both the resting and activated states of the NLRP3 inflammasome during its sustained activation,and targeting HSP90αrepresents a promising therapeutic strategy for diseases driven by the NLRP3 inflammasome.展开更多
Rhizoma Polygoni Cuspidati, a Chinese herbal drug, has actions of dispelling dampness, alleviating jaundice, clearing heat, subsiding toxin, activating blood, and removing stasis. Polydatin （PD）, one of its chief ac...Rhizoma Polygoni Cuspidati, a Chinese herbal drug, has actions of dispelling dampness, alleviating jaundice, clearing heat, subsiding toxin, activating blood, and removing stasis. Polydatin （PD）, one of its chief active ingredients, has been proved by modern pharmacological studies to possess extensive cardiovascular pharmacological activity, showing marked effects on protecting cardio-myocyte, dilating blood vessel, antagonizing platelet aggregation, thrombosis, and atherosclerosis. The progress of the research on cardiovascular pharmacological actions and the acting mechanism of PD was reviewed in this paper.展开更多
Objective: To study the effect of polydatin on p hospholipase A2 in lung tissues in rats with endotoxic shock. Methods: Thirty-two healthy male Wistar rats were employed in this study. A total of 8 rats received norma...Objective: To study the effect of polydatin on p hospholipase A2 in lung tissues in rats with endotoxic shock. Methods: Thirty-two healthy male Wistar rats were employed in this study. A total of 8 rats received normal saline intravenously （control grou p）,8 rats received 10 mg/kg of endotoxin （endotoxic shock group）,8 rats re ceived 1 mg/kg of polydatin after endotoxin injection （polydatin treatment g roup）,and 8 rats received 1 mg/kg of polydatin （polydatin prevention group） 30 minutes before endotoxin injection. Mean arterial pressure was measured once hal f an hour. Lung tissues were collected 6 hours later. Phospholipase A2 activit y was measured with acid titration. The gene expression of secretory phospholipa se A2 type IIA was detected with reverse transcription polymerase chain reacti on. Meanwhile,the histological changes of the lungs among four groups were comp ared through microscopic examination.Results: Phospholipase A2 activity and the gene expression of secretory phospholipase A2 type IIA increased after endotoxin injection,but polydatin could inhibit these effects of endotoxin. Obvious morphological eviden ce could be found in the lung pathological sections and the protective effect of polydatin was most significant in the polydatin prevention group.Conclusions: Polydatin has prophylactic and therapeutic effects （the former is more distinct than the latter） on acutely injured lungs in rats with endotoxic shock and which suggests that polydatin may be a phospholipase A 2 inhibitor.展开更多
文摘AIM To investigate the protective effects of polydatin (PD) against injury to primarily cultured rat hepatocytes induced by CCl 4. METHODS Rat hepatocytes were separated by methods of liver infusion in vivo and cultured medium (7 5×10 5 cells/mL). Two mL or 0 2mL was added into 24 well or 96 well plates respectively. Twenty four hours after cell preculture, PD at concentrations of 10 -7 mol/L-10 -4 mol/L was added into each plate. At the same time injury to hepatocytes was induced by adding 10mmol/L CCl 4. Then, 0 1mL or 1mL culture solution was removed from the 96 well or 24 well plates at 6h , 12h , 24h and 48h after CCl 14 intoxication respectively for the determination of GPT, GSH and MDA. At 48h , the survivability of rat hepatocytes was assayed by the MTT colormetric method. RESULTS After CCl 4 challenge, the release of GPT and the formation of MDA in rat hepatocytes markedly increased and maintained at a high level in 48h , whereas PD with different concentrations could markedly inhibit this elevation with 10 -5 mol/L PD having the strongest effects and inhibiting rate was over 50%. PD could also improve the decreased content of GSH caused by CCl 4 in accordance with the doses used. CCl 4 evidently decreased the hepatocyte survivability from 91 0%±7 9% to 35 4%±3 8%. On the other hand, PD at 10 -7 mol/L-10 -4 mol/L could reverse this change and improve the cell survival rates to 56 1%±5 2%, 65 8%±5 0%, 88 7%±6 8% and 75 2%±7 3%, respectively. CONCLUSION PD at 10 -7 mol/L-10 -4 mol/L could protect primarily cultured rat hepatocytes against CCl 4 induced injury.
基金supported by the National Natural Science Foundation of China,No.81501690(to ZTG)the Scientific Research Staring Foundation for Talent Introduction for Southern Medical University(to MM)
文摘Polydatin is thought to protect mitochondria in different cell types in various diseases.Mitochondrial dysfunction is a major contributing factor in secondary brain injury resulting from traumatic brain injury.To investigate the protective effect of polydatin after traumatic brain injury,a rat brain injury model of lateral fluid percussion was established to mimic traumatic brain injury insults.Rat models were intraperitoneally injected with polydatin(30 mg/kg)or the SIRT1 activator SRT1720(20 mg/kg,as a positive control to polydatin).At 6 hours post-traumatic brain injury insults,western blot assay was used to detect the expression of SIRT1,endoplasmic reticulum stress related proteins and p38 phosphorylation in cerebral cortex on the injured side.Flow cytometry was used to analyze neuronal mitochondrial superoxide,mitochondrial membrane potential and mitochondrial permeability transition pore opened.Ultrastructural damage in neuronal mitochondria was measured by transmission electron microscopy.Our results showed that after treatment with polydatin,release of reactive oxygen species in neuronal mitochondria was markedly reduced;swelling of mitochondria was alleviated;mitochondrial membrane potential was maintained;mitochondrial permeability transition pore opened.Also endoplasmic reticulum stress related proteins were inhibited,including the activation of p-PERK,spliced XBP-1 and cleaved ATF6.SIRT1 expression and activity were increased;p38 phosphorylation and cleaved caspase-9/3 activation were inhibited.Neurological scores of treated rats were increased and the mortality was reduced compared with the rats only subjected to traumatic brain injury.These results indicated that polydatin protectrd rats from the consequences of traumatic brain injury and exerted a protective effect on neuronal mitochondria.The mechanisms may be linked to increased SIRT1 expression and activity,which inhibits the p38 phosphorylation-mediated mitochondrial apoptotic pathway.This study was approved by the Animal Care and Use Committee of the Southern Medical University,China(approval number:L2016113)on January 1,2016.
基金Supported by The Natural Science Foundation of China,No.81271950,to Ji QMProjects of International/HMT(Hong Kong,Macao,and Taiwan)Cooperation and Innovation Platform in Science and Technology of Guangdong Higher Education Institutions,No.2012gjhz0009,to Liu ZG+2 种基金Key Laboratory Construction Program of Shenzhen,No.SW201110010,to Liu ZGBasic Research Program of Shenzhen University,No.201101,to Liu ZGBasic Research Foundation of Shenzhen,No.JC201005250059A,JCYJ20120613115535998
文摘AIM: To investigate the effect of polydatin (PD), a resveratrol glucoside, on mast cell degranulation and antiallergic activity. METHODS: After the rats were orally sensitized with ovalbumin (OVA) for 48 d and underwent PD treatment for 4 d, all the rats were stimulated by 100 mg/mL OVA for24 h and then sacrificed for the following experiments. The small intestines from all the groups were prepared for morphology examination by hematoxylin and eosin staining. We also used a smooth muscle organ bath to evaluate the motility of the small intestines. The OVA-specific immunoglobulin E (IgE) production and interleu-kin-4 (IL-4) levels in serum or supernatant of intestinal mucosa homogenates were analyzed by enzyme-linked immunosorbent assay (ELISA). Using toluidine blue stain, the activation and degranulation of isolated rat peritoneal mast cells (RPMCs) were analyzed. Release of histamine from RPMCs was measured by ELISA, and regulation of PD on intracellular Ca 2+ mobilization was investigated by probing intracellular Ca 2+ with fluo-4 fluo-rescent dye, with the signal recorded and analyzed. RESULTS: We found that intragastric treatment with PD significantly reduced loss of mucosal barrier integrity in the small intestine. However, OVA-sensitization caused significant hyperactivity in the small intestine of allergic rats, which was attenuated by PD administration by 42% (1.26 ± 0.13 g vs OVA 2.18 ± 0.21 g, P < 0.01). PD therapy also inhibited IgE production (3.95 ± 0.53 ng/mL vs OVA 4.53 ± 0.52 ng/mL, P < 0.05) by suppressing the secretion of Th2-type cytokine, IL-4, by 34% (38.58 ± 4.41 pg/mLvs OVA 58.15 ± 6.24 pg/mL, P < 0.01). The ratio of degranulated mast cells, as indicated by vehicles (at least five) around the cells, dramatically increased in the OVA group by 5.5 fold (63.50% ± 15.51% vs phosphate-buffered saline 11.15% ± 8.26%, P < 0.001) and fell by 65% after PD treatment (21.95% ± 4.37% vs OVA 63.50% ± 15.51%, P < 0.001). PD mediated attenuation of mast cell degranulation was further confirmed by decreased histamine levels in both serum (5.98 ± 0.17 vs OVA 6.67 ± 0.12, P < 0.05) and intestinal mucosa homogenates (5.83 ± 0.91 vs OVA 7.35 ± 0.97, P < 0.05). Furthermore, we demonstrated that administration with PD significantly decreased mast cell degranulation due to reduced Ca 2+ influx through store-operated calcium channels (SOCs) (2.35 ± 0.39vs OVA 3.51 ± 0.38,P < 0.01).CONCLUSION: Taken together, our data indicate that PD stabilizes mast cells by suppressing intracellular Ca 2+ mobilization, mainly through inhibiting Ca 2+ entry via SOCs, thus exerting a protective role against OVA-sensitized food allergy.
基金This study was supported by grants from the National Natural Science Foundation of China(No.81970563)the Medical Health Science and Technology Project of Health Commission of Zhejiang Province(2019RC055).
文摘Background:Polydatin,a glucoside of resveratrol,has shown protective effects against various diseases.However,little is known about its effect on hepatic ischemia-reperfusion(I/R)injury.This study aimed to elucidate whether polydatin protects liver against I/R-induced injury and to explore the underlying mechanism.Methods:After gavage feeding polydatin once daily for a week,mice underwent a partial hepatic I/R procedure.Serum alanine aminotransferase(ALT)/aspartate aminotransferase(AST),hematoxylin-eosin(H&E)and TdT-mediated dUTP nick-end labeling(TUNEL)staining were used to evaluate liver injury.The severity related to the inflammatory response and reactive oxygen species(ROS)production was also investigated.Furthermore,immunofluorescence and Western blotting were used to detect macrophage polarization and the NF-κB signaling pathway in macrophages.Results:Compared with the I/R group,polydatin pretreatment significantly attenuated I/R-induced liver damage and apoptosis.The oxidative stress marker(dihydroethidium fluorescence,malondialdehyde,superoxide dismutase and glutathione peroxidase)and I/R related inflammatory cytokines(interleukin1β,interleukin-10 and tumor necrosis factor-α)were significantly suppressed after polydatin treatment.In addition,the result of immunofluorescence indicated that polydatin reduced the polarization of macrophages toward M1 macrophages both in vivo and in vitro.Western blotting showed that polydatin inhibited the pro-inflammatory function of RAW264.7 via down-regulating the NF-κB signaling pathway.Conclusions:Polydatin protects the liver from I/R injury by remodeling macrophage polarization via NFκB signaling.
文摘To investigate the effects of polydatin on the proliferation,migration,and invasion of ovarian cancer,the change of proliferative ability,migration ability,and invasive ability of human ovarian cancer cell OVCAR-3,A2780,and HO-8910 was detected by using polydatin and up-regulating PI3K.The anticancer activity and mechanism of polydatin in ovarian cancer were analyzed.Polydatin could effectively inhibit the proliferation,migration,and invasion of OVCAR-3,A2780,and HO-8910,and inhibit the expression of PI3K protein.After the expression level of PI3K protein was up-regulated,the inhibitory effect of polydatin on the proliferative ability,migration ability,and invasive ability of OVCAR-3,A2780,and HO-8910 significantly decreased,suggesting that PI3K was the target of polydatin.Therefore,we concluded that polydatin could inhibit the proliferation,migration,and invasion of ovarian cancer cells by inhibiting the expression of PI3K protein,which provides an experimental basis for polydatin in the treatment of ovarian cancer.
文摘Objective A method of TLC-fluorescence spectrophotometry was established to assay the content of polydatin in polygonum cuspidatum sieb. et zucc. Methods: Polydatin was extracted by methanol and separated with chloroform-acetone-formic acid-water (4∶4∶0.5∶0.2) by thin layer chromatography. The excitation wavelength and emission wavelength were 284 nm and 384 nm, respectively. Results The linear regression equation of the calibration graph was y=7.02179x+4.5143, a linear regression correlative coefficient r=0.9936. Conclusion This method was proved simple, stable and sensitive. It can be used in quality control of herbs.
基金Project of Traditional Chinese Medicine Administration of Guangxi Zhuang Autonomous Region(GZZC2019147)Project for Improving Basic Research Ability of Middle Aged and Young Teachers in Colleges and Universities of Guangxi in 2020(2020KY13034)+2 种基金The First Batch High-level Talent Scientific Research Project of The Affiliated Hospital of Youjiang Medical University for Nationalities in 2019(Y20196311)National Traditional Chinese Medicine Characteristic Technology Heritage Talent Training Program(2015481601003)Program of Youjiang Medical University for Nationalities(yy2018ky018).
文摘[Objectives]To establish a UPLC-UV method for the determination of polydatin in the serum of Wistar rats.[Methods]Acquity UPLC BEH shield RP18 column(1.7μm,2.1 mm×100 mm,Waters Corporation,USA)was used as the analytical column,acetonitrile-water(55∶45)was used as the mobile phase,the flow rate was 0.5 mL/min,and the column temperature was 30℃and the detection wavelength was 306 nm.[Results]The linear range of the established serum sample analysis method was 1.0-20.0μg/mL,and the correlation coefficient was r=0.9994;the intraday and interday RSD of Wistar rat serum was less than 3.0%,and the accuracy was higher than 90%.[Conclusions]This method is sensitive,accurate,and rapid.It is suitable for monitoring the concentration of polydatin in serum after intragastric administration,and can also be used for pharmacokinetics and bioavailability studies.
文摘Rheumatological diseases encompass a wide range of conditions primarily affecting the musculoskeletal system.They represent a significant burden on modern society,affecting millions of people worldwide.These chronic and debilitating conditions require long-term management and a multidisciplinary approach that combines pharmacological interventions with lifestyle modifications for optimal patient outcomes.In this context,diet is emerging as a crucial support in managing rheumatological diseases.Certain dietary patterns and specific nu-trients can play a significant role in reducing inflammation,alleviating symptoms,and potentially slowing disease progression.Bioactive compounds,which are found in many plant-based foods and are abundant in the Mediterranean diet,are increasingly being recognized as valuable supports to traditional treatments in arthritis.Among them,polydatin has shown potent antioxidant and anti-inflammatory properties.This review aims to comprehensively examine the therapeutic potential of polydatin in various rheumato-logical diseases,including rheumatoid arthritis,osteoarthritis,crystal-induced arthritis,spondyloarthritis,and systemic lupus erythematosus.Articles included have been identified using keyword-based searches in multiple scientific databases,including PubMed and Scopus.The review highlights polydatin's multi-targeted mechanisms,including antioxidant activity,modulation of inflammatory pathways,regulation of apoptosis and autophagy,and direct interactions with molecular targets like sirtuin 1 and chemokine receptor type 1.Although clinical studies specifically investigating polydatin in rheumatological conditions are scarce,the translational potential of this compound is supported by randomized controlled trials involving other human inflammatory and pain-related disorders.Polydatin's favorable phar-macokinetic profile,enhanced bioavailability,and diverse biological actions position it as a promising natural compound for managing rheumatological diseases.
基金supported by the National Natural Science Founda-tion of China(NSFC,Grant No.82301650)the Scientific Research Project of Wuhan Polytechnic University(Grant No.2023Y66)the Scientific Research Project of Wuhan Polytechnic University(Grant No.2023RZ037).
文摘This study investigated the antiepileptic effects of polydatin(PD)and its potential mechanisms.Racine scoring and EEG were used to assess seizure severity in a PTZ-induced mouse epilepsy model.The results demonstrated that PD significantly reduced the intensity of seizures.Behavioral tests revealed that PD improved learning,memory,and motor coordination.Histological analysis using HE and Nissl staining showed that PD alleviated hippocampal neuronal damage.TUNEL staining further confirmed that PD effectively prevented neuronal apoptosis.Network pharmacology predicted SIRT1 as a potential target of PD,and GO and KEGG pathway enrichment analyses indicated that PD regulated mitochondrial function.Therefore,PD may reduce neuronal damage by protecting mitochondrial function through SIRT1.This process was tested both in vitro and in vivo.In a Mg^(2+)-free neuronal excitability model,CCK-8,LDH,and Hoechst staining results demonstrated that PD significantly increased cell survival and reduced apoptosis.Reduced mitosox staining,along with increased activity of Complexes IV and V and ATP production,indicated that PD mitigated mitochondrial function.Gene expression studies revealed that PD activated the SIRT1-PGC-1αsignaling pathway via AMPK.In conclusion,PD exerted neuroprotective effects by regulating mitochondrial function,suggesting a potential therapeutic target for epilepsy.
基金supported by the National Natural Science Foundation of China(82273933,82073856,82230116,and 82473929)Innovation Team and Talents Cultivation Program of National Administration of Traditional Chinese Medicine(no.ZYYCXTD-C-202208)Fundamental Research Funds for the Central Universities(020814380199).
文摘The NLRP3 inflammasome plays a critical role in various inflammatory conditions.However,despite extensive research in targeted drug development for NLRP3,including MCC950,clinical success remains elusive.Here,we discovered that the activated NLRP3 inflammasome complex(disc-NLRP3)and the activating mutation L351P exhibited resistance to MCC950.Through investigations using the small-molecule compound polydatin,HSP90αwas found to stabilize both the resting(cage-NLRP3)and activated state(disc-NLRP3)of NLRP3 complexes,sustaining its activation.Our mechanistic studies revealed that polydatin specifically targets HSP90α,binding to it directly and subsequently interfering with the HSP90α-NLRP3 interaction.This disruption leads to the dissipation of cage-NLRP3,disc-NLRP3 complexes and NLRP3 L351P.Importantly,genetic and pharmacological inactivation of HSP90αeffectively reduced NLRP3 inflammasome activation and alleviated cerulein-induced acute pancreatitis.These therapeutic effects highlight the clinical potential of HSP90αinhibition.Our findings demonstrate that HSP90αis crucial for the stability of both the resting and activated states of the NLRP3 inflammasome during its sustained activation,and targeting HSP90αrepresents a promising therapeutic strategy for diseases driven by the NLRP3 inflammasome.
基金Supported by the National Natural Science Foundation of China(No.81102721)A Planned Technologic Item of State Administration of Traditional Chinese Medicine(No 04-05LP30)+2 种基金Chinese National Scientific Fund for Post-doctor(No 20070410622)Its Special Aid ltem(No.201003226)the Key Technologies R&D Program of Shandong Province(No 2010 GSF 10289)
文摘Rhizoma Polygoni Cuspidati, a Chinese herbal drug, has actions of dispelling dampness, alleviating jaundice, clearing heat, subsiding toxin, activating blood, and removing stasis. Polydatin （PD）, one of its chief active ingredients, has been proved by modern pharmacological studies to possess extensive cardiovascular pharmacological activity, showing marked effects on protecting cardio-myocyte, dilating blood vessel, antagonizing platelet aggregation, thrombosis, and atherosclerosis. The progress of the research on cardiovascular pharmacological actions and the acting mechanism of PD was reviewed in this paper.
文摘Objective: To study the effect of polydatin on p hospholipase A2 in lung tissues in rats with endotoxic shock. Methods: Thirty-two healthy male Wistar rats were employed in this study. A total of 8 rats received normal saline intravenously （control grou p）,8 rats received 10 mg/kg of endotoxin （endotoxic shock group）,8 rats re ceived 1 mg/kg of polydatin after endotoxin injection （polydatin treatment g roup）,and 8 rats received 1 mg/kg of polydatin （polydatin prevention group） 30 minutes before endotoxin injection. Mean arterial pressure was measured once hal f an hour. Lung tissues were collected 6 hours later. Phospholipase A2 activit y was measured with acid titration. The gene expression of secretory phospholipa se A2 type IIA was detected with reverse transcription polymerase chain reacti on. Meanwhile,the histological changes of the lungs among four groups were comp ared through microscopic examination.Results: Phospholipase A2 activity and the gene expression of secretory phospholipase A2 type IIA increased after endotoxin injection,but polydatin could inhibit these effects of endotoxin. Obvious morphological eviden ce could be found in the lung pathological sections and the protective effect of polydatin was most significant in the polydatin prevention group.Conclusions: Polydatin has prophylactic and therapeutic effects （the former is more distinct than the latter） on acutely injured lungs in rats with endotoxic shock and which suggests that polydatin may be a phospholipase A 2 inhibitor.
