Oncology Research Editorial Office Published:19 January 2026 The published article titled“miR-202 Promotes Cell Apoptosis in Esophageal Squamous Cell Carcinoma by Targeting HSF2”has been retracted from Oncology Rese...Oncology Research Editorial Office Published:19 January 2026 The published article titled“miR-202 Promotes Cell Apoptosis in Esophageal Squamous Cell Carcinoma by Targeting HSF2”has been retracted from Oncology Research,Vol.25,No.2,2017,pp.215-223.DOI:10.3727/096504016X14732772150541 URL:https://www.techscience.com/or/v25n2/56800.展开更多
Objectives Glioblastoma multiforme(GBM)is highly resistant to apoptosis.This study investigates the role of Selenoprotein M(SELENOM),a redox-regulating protein,in the response of human glioblastoma A-172 cells to stau...Objectives Glioblastoma multiforme(GBM)is highly resistant to apoptosis.This study investigates the role of Selenoprotein M(SELENOM),a redox-regulating protein,in the response of human glioblastoma A-172 cells to staurosporine(STS)and hyperthermia.Methods A stable SELENOM-knockdown(SELENOM-KD)cell line was created.We measured reactive oxygen species(ROS),mitochondrial membrane potential(ΔΨm),cell death,and apoptotic gene expression.Results SELENOM-KD increased basal ROS levels and induced mitochondrial dysfunction.It sensitized cells to STS-induced apoptosis,enhancing the upregulation of pro-apoptotic genes.Conversely,under hyperthermia(42°C),SELENOM-KD cells exhibited significant thermoresistance,with 52%survival vs.99%death in controls,associated with suppressed pro-apoptotic signaling.Conclusions SELENOM is a critical redox and mitochondrial regulator in GBM.Its loss produces a context-dependent effect on cell fate:sensitizing to chemical apoptosis while conferring resistance to hyperthermia.SELENOM expression is a promising predictive biomarker for stratifying GBM patients for hyperthermia-based therapies.展开更多
Regulation of apoptosis represents a key parameter in all living organisms.In this paper,an input-induced logic-gated modular nanocalculator is designed to regulate cancer cell apoptosis by programmatically combining ...Regulation of apoptosis represents a key parameter in all living organisms.In this paper,an input-induced logic-gated modular nanocalculator is designed to regulate cancer cell apoptosis by programmatically combining and connecting logic gate modules with different functions.Via rational design of the various logic gate modules of the nanocalculator,different apoptosis related operations including cancer cell targeting,apoptosis induction,and apoptosis monitoring could be performed.Importantly,each of these logic gate modules could independently perform apoptosis related YES logic operations when ran separately.After combining each YES logic gate module into a logic circuit and connecting it to the GO scaffold to construct a logic-gated nanocalculator,the input-induced logic-gated modular nanocalculator could selectively enter cancer cells and control the drug release to logically apoptosis(output),by performing AND logic gate operations when inputs(nucleolin and H^(+)) were included at the same time.Moreover,evidence suggests that these efficient logical calculations proceed in cancer cell apoptosis regulation without the general limiations of lithography in nanotechnology.As such,this work provides a new vision for the construction of a logic-gated modular nanocalculator with logical calculation proficiency potentially useful in cancer therapy and the regulation of life.展开更多
Background:Parkinson’s disease(PD)is one of the most common movement disorders worldwide.Ziyin Xifeng Decoction(ZYXFD),a traditional Chinese medicine compound formula,has shown therapeutic efficacy in treating PD,but...Background:Parkinson’s disease(PD)is one of the most common movement disorders worldwide.Ziyin Xifeng Decoction(ZYXFD),a traditional Chinese medicine compound formula,has shown therapeutic efficacy in treating PD,but its specific mechanisms of action have not been fully elucidated.Methods:Firstly,we employed network pharmacology and untargeted metabolomics analysis to identify the core targets,pathways,and key metabolites of ZYXFD in the treatment of PD.Subsequently,we evaluated the protective effects of ZYXFD and further investigated its anti-PD mechanisms by validating the analytical results.Results:Combined analyses of network pharmacology and metabolomics identify the core targets including EGFR,SRC,PTGS2,and CDK2,while the effects of ZYXFD against PD are likely mediated primarily through the PI3K/AKT/mTOR signaling pathway.Pharmacodynamic evaluation demonstrated that a high dose of ZYXFD significantly improved behavioral deficits in chronic PD mice,downregulatedα-synuclein protein expression,and protected dopaminergic neurons.It also regulated the expression of core targets,inhibited the PI3K/AKT/mTOR signaling pathway,promoted autophagy,and reduced apoptosis.In vitro experiments further verified that the therapeutic effect of ZYXFD on PD is dependent on autophagy regulation.Conclusion:The findings demonstrated that ZYXFD alleviates PD by modulating related proteins and metabolites,inhibiting the PI3K/AKT/mTOR signaling pathway,and enhancing autophagy.This provides a theoretical basis for its broader application in PD treatment.展开更多
Objective:To assess the antitumor activity of the novel chitinase produced by fermented,isolated Trichoderma viride in a hepatocellular carcinoma(HCC)male rat model.Methods:Diethyl-nitrosamine induction combined with ...Objective:To assess the antitumor activity of the novel chitinase produced by fermented,isolated Trichoderma viride in a hepatocellular carcinoma(HCC)male rat model.Methods:Diethyl-nitrosamine induction combined with ionizing radiation exposure was used to establish the HCC rat model.All rats were divided into 4 groups:the control group,the chitinase group,the HCC group,and the HCC+chitinase group.The antiproliferative effect of chitinase was evaluated in human HCC cells.The effect of chitinase in vivo on oxidative stress,endoplasmic reticulum stress chaperones,autophagy markers,PI3K/AKT/mTOR,AMPK pathway expression,and apoptotic indicators was determined and confirmed by histological examination.Results:Chitinase significantly inhibited the viabilities of HepG2 cells.Moreover,in the Wistar male rat model of HCC,chitinase decreased ATP levels,modulated endoplasmic reticulum stress,mediated autophagy factors,and promoted apoptosis.Conclusions:Chitinase might play a role in the apoptosis as well as autophagy pathways and may act as a potential tumor suppressor.展开更多
In vivo imaging of neurodegenerative diseases provides valuable insights into disease mechanisms and potential therapeutic interventions.Many ocular diseases are closely linked to neurodegenerative conditions affectin...In vivo imaging of neurodegenerative diseases provides valuable insights into disease mechanisms and potential therapeutic interventions.Many ocular diseases are closely linked to neurodegenerative conditions affecting the brain,making the eye a unique and accessible model for studying these disorders.The transparency of eyes allows researchers to monitor disease progression non-invasively,offering a window into neural health.展开更多
Oncology Research Editorial Office Published:19 January 2026 The published article titled“miR-126-5p Restoration Promotes Cell Apoptosis in Cervical Cancer by Targeting Bcl2l2”has been retracted from Oncology Resear...Oncology Research Editorial Office Published:19 January 2026 The published article titled“miR-126-5p Restoration Promotes Cell Apoptosis in Cervical Cancer by Targeting Bcl2l2”has been retracted from Oncology Research,Vol.25,No.4,2017,pp.463-470.DOI:10.3727/096504016X14685034103879 URL:https://www.techscience.com/or/v25n4/56826.展开更多
Post-translational modifications(PTMs)regulate the occurrence and development of cancer,and lactylation modification is a new form of PTMs.Recent studies have found that lactic acid modification can regulate the immun...Post-translational modifications(PTMs)regulate the occurrence and development of cancer,and lactylation modification is a new form of PTMs.Recent studies have found that lactic acid modification can regulate the immune tolerance of cancer cells.The classical theory holds that prostate apoptosis response-4(PAR-4)is a tumor suppressor protein.However,our recent research has found that PAR-4 has a biological function of promoting cancer in hepatocellular carcinoma(HCC),and our analysis shows that PAR-4 can be modified of lactic acid.These research evidences suggest that PAR-4 lactylation modification may drive immune tolerance in HCC.Therefore,inhibiting PAR-4 lactylation modification is very likely to increase the sensitivity of HCC to immunotherapy.展开更多
Temporomandibular joint osteoarthritis(TMJ-OA) affects a significant proportion of the population worldwide.However,there has been no substantial progress in the development of FDA-approved drugs for treatment due to ...Temporomandibular joint osteoarthritis(TMJ-OA) affects a significant proportion of the population worldwide.However,there has been no substantial progress in the development of FDA-approved drugs for treatment due to a lack of understanding of the specific factors regulating key TMJ-OA molecular mechanisms.Lysyl Oxidase-Like-2(LOXL2) promotes knee joint cartilage protection and is down regulated in a TMJ-OA animal model.We evaluated the role of LOXL2 in TMJ cartilage,its molecular mechanism,and gene networks using in vivo Loxl2 knockout mice(Acan-Cre;Loxl2^(flox/flox)) and ex vivo goat TMJ cartilage.Our results show that Loxl2 knockout in mouse cartilage upregulates Il1b,Mmp9,Mmp13,Adamts4,and Adamts5,but reduces the levels of aggrecan and proteoglycan.Loxl2 deleted TMJ cartilage show a higher enrichment of inflammatory response,TNFA signaling via NF-κB,extracellular matrix(ECM),and collagen degradation pathway network.Conversely,LOXL2 treatment reduces interleukin-1beta(IL-1β)-induced expression of Mmp13,protects mitochondrial function,and ECM from degeneration.Importantly,LOXL2attenuates IL-1 β-induced chondrocyte apoptosis via the phosphorylation of NF-κB and expression of the pain-related gene PTGS2(encodes COX2).Taken together,Loxl2 knockout mice exacerbate TMJ-OA through cartilage/ECM degradation,mitochondrial dysfunction,chondrocyte apoptosis,and inflammatory gene expression,whereas LOXL2 treatment mitigate these effects.展开更多
Nekemias megalophylla is a popular folk tea consumed by people in the Western Hubei(China)of which ampelopsin(AMP)is the main active ingredient.In this study,we investigated the effect of AMP on cervical cancer and ex...Nekemias megalophylla is a popular folk tea consumed by people in the Western Hubei(China)of which ampelopsin(AMP)is the main active ingredient.In this study,we investigated the effect of AMP on cervical cancer and explored its mechanism of action,focusing on apoptosis and autophagy.Firstly,we verified that AMP strongly inhibited the growth of C-33A cells and observed apoptosis and autophagy phenomenon in vivo,and found that AMP induces C-33A cell apoptosis via death receptor or mitochondrial pathways.The results also indicated that AMP-induced autophagy occurs via the PI3K/Akt/m TOR pathway.Secondly,when autophagy was inhibited,the AMP-induced apoptosis of C-33A cells was strengthened,when apoptosis was inhibited,the AMP-induced autophagy of C-33A cells was strengthened.PI3K/Akt/m TOR pathway activation enhances AMP-induced apoptosis in C-33A cells,while its inhibition strengthens AMP-induced autophagy.Finally,we confirmed that AMP inhibited cell growth and induced apoptosis and autophagy of C-33A cells in an in vivo nude mouse model of C-33A tumor xenografts.These results elucidate that AMP bidirectionally regulates apoptosis and autophagy in human cervical cancer C-33A cells by mediating the PI3K/Akt/m TOR pathway.展开更多
Crosstalk between the nervous system and cancer plays an important role in tumor metastasis yet is poorly understood.Recently,Padmanaban et al.demonstrated a novel mechanism for nerve-induced metastasis.Sensory nerve-...Crosstalk between the nervous system and cancer plays an important role in tumor metastasis yet is poorly understood.Recently,Padmanaban et al.demonstrated a novel mechanism for nerve-induced metastasis.Sensory nerve-derived substance P could induce apoptosis in breast cancer cells that overexpressed tachykinin receptors.Single-stranded RNAs(ssRNAs)leaking from dying cells subsequently interact with toll-like receptor 7(TLR7)on other cancer cells and finally promoted metastasis.This notable study displays a delicate loop between the nervous system and cancer and,more importantly,amplifies the conception of apoptosis-induced metastasis.Over the past years,a mass of breakthrough studies have proven the pivotal role of the nervous system in tumorigenesis and cancer progression thereby contributing to the creation of a new disciplinecancer neuroscience[1].Hanahan and Monje discussed in detail the interactions between the nervous system and tumors based on the theoretical framework of the cancer hallmarks,focused on nerve-mediated proliferation,angiogenesis,immune evasion,cell death resistance,and metastasis[2].展开更多
The published article titled“MicroRNA-98-5p Inhibits Cell Proliferation and Induces Cell Apoptosis in Hepatocellular Carcinoma via Targeting IGF2BP1”has been retracted from Oncology Research,Vol.25,No.7,2017,pp.1117...The published article titled“MicroRNA-98-5p Inhibits Cell Proliferation and Induces Cell Apoptosis in Hepatocellular Carcinoma via Targeting IGF2BP1”has been retracted from Oncology Research,Vol.25,No.7,2017,pp.1117–1127.展开更多
The aim of this study is to investigate the mechanism of magnesium isoglycyrrhizinate(MgIG)in the treatment of myocardial remodeling induced by isoproterenol(ISO)in mice.We assessed the impact of MgIG on ISO-induced m...The aim of this study is to investigate the mechanism of magnesium isoglycyrrhizinate(MgIG)in the treatment of myocardial remodeling induced by isoproterenol(ISO)in mice.We assessed the impact of MgIG on ISO-induced myocardial remodeling by activating the PI3K/AKT1 pathway.The cardiac function of mice was evaluated by echocardiography,revealing that MgIG could improve left ventricular function.Pathological staining analysis showed that MgIG could reduce the degree of myocardial injury caused by ISO.Serum data detected by ELISA demonstrated that MgIG could decrease the levels of CK-MB,MDA,and LDH while increasing the activity of GSH-Px.Western blotting analysis revealed that protein expression levels of Collagen I,BNP,Bax,cleaved caspase-3,p-PI3K,and p-AKT1 were decreased,whereas the protein expressions of Bcl-2,COX2,and SOD1 were increased upon MgIG treatment.However,the activation of the PI3K pathway reversed the cardioprotective effects of MgIG,as evidenced by the addition of PI3K activators.Taken together,our comprehensive results suggested that MgIG could improve ISO-induced myocardial remodeling,potentially through its mechanism of inhibiting the PI3K/AKT1 pathway to regulate apoptosis and oxidative stress.展开更多
Objective Emerging evidence suggests that exposure to ultrafine particulate matter(UPM,aerodynamic diameter<0.1μm)is associated with adverse cardiovascular events.Previous studies have found that Shenlian(SL)extra...Objective Emerging evidence suggests that exposure to ultrafine particulate matter(UPM,aerodynamic diameter<0.1μm)is associated with adverse cardiovascular events.Previous studies have found that Shenlian(SL)extract possesses anti-inflammatory and antiapoptotic properties and has a promising protective effect at all stages of the atherosclerotic disease process.In this study,we aimed to investigated whether SL improves UPM-aggravated myocardial ischemic injury by inhibiting inflammation and cell apoptosis.Methods We established a mouse model of MI+UPM.Echocardiographic measurement,measurement of myocardialinfarct size,biochemical analysis,enzyme-linked immunosorbent assay(ELISA),histopathological analysis,Transferase dUTP Nick End Labeling(TUNEL),Western blotting(WB),Polymerase Chain Reaction(PCR)and so on were used to explore the anti-inflammatory and antiapoptotic effects of SL in vivo and in vitro.Results SL treatment can attenuate UPM-induced cardiac dysfunction by improving left ventricular ejection fraction,fractional shortening,and decreasing cardiac infarction area.SL significantly reduced the levels of myocardial enzymes and attenuated UPM-induced morphological alterations.Moreover,SL significantly reduced expression levels of the inflammatory cytokines IL-6,TNF-α,and MCP-1.UPM further increased the infiltration of macrophages in myocardial tissue,whereas SL intervention reversed this phenomenon.UPM also triggered myocardial apoptosis,which was markedly attenuated by SL treatment.The results of in vitro experiments revealed that SL prevented cell damage caused by exposure to UPM combined with hypoxia by reducing the expression of the inflammatory factor NF-κB and inhibiting apoptosis in H9c2 cells.Conclusion Overall,both in vivo and in vitro experiments demonstrated that SL attenuated UPMaggravated myocardial ischemic injury by inhibiting inflammation and cell apoptosis.The mechanisms were related to the downregulation of macrophages infiltrating heart tissues.展开更多
Diabetic kidney disease(DKD)has a high incidence and mortality rate and lacks effective preventive and therapeutic methods.Apoptosis is one of the main reasons for the occurrence and development of DKD.Mesenchymal ste...Diabetic kidney disease(DKD)has a high incidence and mortality rate and lacks effective preventive and therapeutic methods.Apoptosis is one of the main reasons for the occurrence and development of DKD.Mesenchymal stem cells(MSCs)have shown great promise in tissue regeneration for DKD treatment and have protective effects against DKD,including decreased blood glucose and urinary protein levels and improved renal function.MSCs can directly differ-entiate into kidney cells or act via paracrine mechanisms to reduce apoptosis in DKD by modulating signaling pathways.MSC-derived extracellular vesicles(MSC-EVs)mitigate apoptosis and DKD-related symptoms by transferring miRNAs to target cells or organs.However,studies on the regulatory mechanisms of MSCs and MSC-EVs in apoptosis in DKD are insufficient.This review compre-hensively examines the mechanisms of apoptosis in DKD and research progress regarding the roles of MSCs and MSC-EVs in the disease process.展开更多
Background Higher embryonic mortality,especially in aged breeding hens,is associated with insufficient hepatic functionality in maintaining redox homeostasis.Our previous study demonstrated that egg exosome-derived mi...Background Higher embryonic mortality,especially in aged breeding hens,is associated with insufficient hepatic functionality in maintaining redox homeostasis.Our previous study demonstrated that egg exosome-derived miRNAs may play a key role in modulating embryonic oxidation-reduction process,whereas the exact function and mechanism were still poorly understood.The present study aimed to investigate the roles of egg exosome miRNAs in maintaining dynamic equilibrium of free radicals and peroxide agents in embryonic liver,as well as demonstrate the specific mechanism using oxidative stress-challenged hepatocytes.Results Compared to 36-week-old breeding hens,decreased hatchability and increased embryonic mortality were observed in 65-week-old breeding hens.Meanwhile,the older group showed the increased MDA levels and decreased SOD and GSH-Px activities in embryonic liver,muscle and serum.Embryonic mortality was significantly positively correlated with MDA level and negatively correlated with GSH-Px activity in embryonic liver.In addition,363 differentially expressed genes(DEGs)were identified in embryonic liver,13 differentially expressed miRNAs(DE-miRNAs)were identified in egg exosomes.These DEGs and DE-miRNAs were involved in oxidoreductase activity,glutathione metabolic process,MAPK signaling pathway,apoptosis and autophagy.miRNA-mRNA network analysis further found that DEGs targeted by DE-miRNAs were mainly enriched in programmed cell death,such as apoptosis and autophagy.Wherein,MAPK10 with highest MCC and AUC values was significantly related to GSH-Px activity and MDA level,and served as the target gene of miR-145-5p based on dual luciferase reporter experiment and correlation analysis.Bioinformatics analysis found that miR-145-5p/MAPK10 axis might alleviate peroxide generation and apoptosis.In primary hepatocytes of chick embryos,miR-145-5p transfection significantly reversed H_(2)O_(2)-induced mitochondrial ROS increase,MAPK10,BAX and CASP3 overexpression and excessive apoptosis.Conclusion Exosome miR-145-5p in eggs could target MAPK10 and decrease mitochondrial ROS,attenuating oxidative damage and apoptosis in hepatocytes of chick embryos.These findings may provide new theoretical basis for the improvement of maternal physiological status to maintain embryonic redox homeostasis by nutritional or genetic modifications.展开更多
Background:The outcomes of pediatric patients with acute lymphoblastic leukemia(ALL)remain far less than favorable.While apigenin is an anti-cancer agent,studies on the mechanism by which it regulates ALL cell cycle p...Background:The outcomes of pediatric patients with acute lymphoblastic leukemia(ALL)remain far less than favorable.While apigenin is an anti-cancer agent,studies on the mechanism by which it regulates ALL cell cycle progression are inadequate.Ferroptosis and AMP-activated protein kinase(AMPK)signaling are important processes for ALL patients.However,it remains unclear whether apigenin works by affecting AMPK and apoptosis.Materials and Methods:SUP-B15 and T-cell Jurkat ALL cells were treated with apigenin,and cell viability and apoptosis were measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)and terminal deoxynucleotidyl transferase dUTP nick end labeling(TUNEL)assays,respectively.The thiobarbituric acid-reactive substances(TBARS)assay was used to evaluate lipid peroxidation.Intracellular Fe2+levels were measured using a commercial kit.Corresponding proteins were detected by western blotting.Results:Results showed that apigenin reduced cell viability and the levels of Ki67 and proliferating cell nuclear antigen(PCNA)expression in a concentration-dependent manner in both types of ALL cells.Apigenin also exerted anti-apoptotic effects on SUP-B15 and Jurkat cells.Apigenin activated AMP-activated protein kinase(AMPK)signaling and induced ferroptosis,and those effects were attenuated by inhibition of AMPK.Eventually,the reduced cell proliferation and increased cell apoptosis caused by apigenin in ALL cells were partly abolished by AMPK inhibition.Conclusion:In summary,apigenin exerted anti-leukemia activity in ALL cells,and that effect was partially achieved by activation of AMPK signaling.Our findings suggest apigenin as a potential drug for treatment of ALL.展开更多
OBJECTIVE:To investigate the effect and mechanism of Yishen Tongluo formula(益肾通络方,YSTLF)in streptozotocin-induced diabetic kidney disease mice(DKD)mice.METHODS:Thirty Institute of Cancer Research mice(specific pa...OBJECTIVE:To investigate the effect and mechanism of Yishen Tongluo formula(益肾通络方,YSTLF)in streptozotocin-induced diabetic kidney disease mice(DKD)mice.METHODS:Thirty Institute of Cancer Research mice(specific pathogen free,SPF grade)were divided into five groups(n=6 per group):control,DKD model,DKD model with YSTLF(4.9 g/kg),DKD model with YSTLF(9.8 g/kg),and DKD model with captopril.DKD was induced through a single intraperitoneal injection of streptozotocin(150 mg/kg).Body weight,fasting blood glucose and urine C-peptide levels were measured to assess metabolic regulation by YSTLF.Renal function was evaluated using indicators of glomerular and tubular health.Liver function was assessed by measuring aspartate aminotransferase and alanine aminotransferase levels.Renal pathological changes were examined using hematoxylin/eosin staining and transmission electron microscopy.Inflammatory and apoptosis-related factors were analyzed through enzyme-linked immunosorbent assay,immunohistochemistry,and Western blot analysis.RESULTS:In DKD mice,fasting blood glucose,Cpeptide,24-hour urine protein(UP)levels,and renal damage were elevated,accompanied by increased inflammation and apoptosis.YSTLF significantly reduced 24-hour UP and C-peptide levels and improved kidney and liver function in DKD mice.YSTLF also mitigated glomerular hypertrophy,basement membrane thickening,and podocyte foot process effacement.It upregulated the expression of the podocyte marker podocalyxin.Furthermore,YSTLF alleviated inflammation and apoptosis,likely by reducing the overexpression of monocyte chemoattractant protein(MCP-1),Bax,and Caspase-3 in the kidneys of DKD mice.CONCLUSIONS:These findings suggest that YSTLF ameliorates kidney injury by modulating the expression of inflammatory cytokine MCP-1 and the Bax/Caspase-3 apoptosis pathway,providing a potential therapeutic approach for DKD.展开更多
Myocardial ischemia(MI)is a pathophysiological condition in which the myocardium is unable to maintain normal cardiac function due to insufficient coronary artery blood and oxygen supply,as well as abnormal myocardial...Myocardial ischemia(MI)is a pathophysiological condition in which the myocardium is unable to maintain normal cardiac function due to insufficient coronary artery blood and oxygen supply,as well as abnormal myocardial energy metabolism[1].Ginsenoside Rbi(Rbi),one of the most abundant natural ingredients in ginseng and Panax notoginseng,has been proven to protect the heart from MI/reperfusion injury(RI)[2].展开更多
Artemisia annua L.is a medicinal herb with multiple therapeutic applications,whereas its antiinfluenza A virus(IAV)efficiency and mechanism of action are still unclear.Here,we investigated the inhibition activity and ...Artemisia annua L.is a medicinal herb with multiple therapeutic applications,whereas its antiinfluenza A virus(IAV)efficiency and mechanism of action are still unclear.Here,we investigated the inhibition activity and mechanism of A.annua leaf methanol extracts(AALME)against IAV in vitro and in vivo.Our results revealed that AALME exhibits potent anti-IAV activity by interacting with IAV particles.Mechanistically,AALME directly targets the IAV nucleoprotein(NP)protein and abolishes the nuclear import of IAV NP.AALME profoundly suppresses IAV-induced mitochondrial apoptosis via suppressing ROS-mediated AIF-dependent pathways.More importantly,we found that AALME plays a crucial role in protecting mice from IAV infection and mitigating IAV pathogenicity.This current work provides mechanistic insight into the mechanism by which AALME controls IAV infection in vitro and in vivo,potentially contributing to the development of antiviral treatments for IAV infection.展开更多
文摘Oncology Research Editorial Office Published:19 January 2026 The published article titled“miR-202 Promotes Cell Apoptosis in Esophageal Squamous Cell Carcinoma by Targeting HSF2”has been retracted from Oncology Research,Vol.25,No.2,2017,pp.215-223.DOI:10.3727/096504016X14732772150541 URL:https://www.techscience.com/or/v25n2/56800.
基金the framework of the State assignment No.075-00607-25-00.
文摘Objectives Glioblastoma multiforme(GBM)is highly resistant to apoptosis.This study investigates the role of Selenoprotein M(SELENOM),a redox-regulating protein,in the response of human glioblastoma A-172 cells to staurosporine(STS)and hyperthermia.Methods A stable SELENOM-knockdown(SELENOM-KD)cell line was created.We measured reactive oxygen species(ROS),mitochondrial membrane potential(ΔΨm),cell death,and apoptotic gene expression.Results SELENOM-KD increased basal ROS levels and induced mitochondrial dysfunction.It sensitized cells to STS-induced apoptosis,enhancing the upregulation of pro-apoptotic genes.Conversely,under hyperthermia(42°C),SELENOM-KD cells exhibited significant thermoresistance,with 52%survival vs.99%death in controls,associated with suppressed pro-apoptotic signaling.Conclusions SELENOM is a critical redox and mitochondrial regulator in GBM.Its loss produces a context-dependent effect on cell fate:sensitizing to chemical apoptosis while conferring resistance to hyperthermia.SELENOM expression is a promising predictive biomarker for stratifying GBM patients for hyperthermia-based therapies.
基金financially supported by the National Natural Science Foundation of China (NSFC,Nos.22134005 and 22074124)Chongqing Talents Program for Outstanding Scientists (No.cstc2021ycjh-bgzxm0178)+1 种基金Natural Science Foundation of Chongqing (No.CSTB2022NSCQ-MSX0521)the Chongqing Graduate Student Scientific Research Innovation Project (No.CYB21119)。
文摘Regulation of apoptosis represents a key parameter in all living organisms.In this paper,an input-induced logic-gated modular nanocalculator is designed to regulate cancer cell apoptosis by programmatically combining and connecting logic gate modules with different functions.Via rational design of the various logic gate modules of the nanocalculator,different apoptosis related operations including cancer cell targeting,apoptosis induction,and apoptosis monitoring could be performed.Importantly,each of these logic gate modules could independently perform apoptosis related YES logic operations when ran separately.After combining each YES logic gate module into a logic circuit and connecting it to the GO scaffold to construct a logic-gated nanocalculator,the input-induced logic-gated modular nanocalculator could selectively enter cancer cells and control the drug release to logically apoptosis(output),by performing AND logic gate operations when inputs(nucleolin and H^(+)) were included at the same time.Moreover,evidence suggests that these efficient logical calculations proceed in cancer cell apoptosis regulation without the general limiations of lithography in nanotechnology.As such,this work provides a new vision for the construction of a logic-gated modular nanocalculator with logical calculation proficiency potentially useful in cancer therapy and the regulation of life.
基金funded by Zhejiang Province Traditional Chinese Medicine Science and Technology Program(No.2021ZZ012)The Changlin Qiu National Distinguished Senior Traditional Chinese Medicine Expert Heritage Workshop Project(No.GZS2021007).
文摘Background:Parkinson’s disease(PD)is one of the most common movement disorders worldwide.Ziyin Xifeng Decoction(ZYXFD),a traditional Chinese medicine compound formula,has shown therapeutic efficacy in treating PD,but its specific mechanisms of action have not been fully elucidated.Methods:Firstly,we employed network pharmacology and untargeted metabolomics analysis to identify the core targets,pathways,and key metabolites of ZYXFD in the treatment of PD.Subsequently,we evaluated the protective effects of ZYXFD and further investigated its anti-PD mechanisms by validating the analytical results.Results:Combined analyses of network pharmacology and metabolomics identify the core targets including EGFR,SRC,PTGS2,and CDK2,while the effects of ZYXFD against PD are likely mediated primarily through the PI3K/AKT/mTOR signaling pathway.Pharmacodynamic evaluation demonstrated that a high dose of ZYXFD significantly improved behavioral deficits in chronic PD mice,downregulatedα-synuclein protein expression,and protected dopaminergic neurons.It also regulated the expression of core targets,inhibited the PI3K/AKT/mTOR signaling pathway,promoted autophagy,and reduced apoptosis.In vitro experiments further verified that the therapeutic effect of ZYXFD on PD is dependent on autophagy regulation.Conclusion:The findings demonstrated that ZYXFD alleviates PD by modulating related proteins and metabolites,inhibiting the PI3K/AKT/mTOR signaling pathway,and enhancing autophagy.This provides a theoretical basis for its broader application in PD treatment.
文摘Objective:To assess the antitumor activity of the novel chitinase produced by fermented,isolated Trichoderma viride in a hepatocellular carcinoma(HCC)male rat model.Methods:Diethyl-nitrosamine induction combined with ionizing radiation exposure was used to establish the HCC rat model.All rats were divided into 4 groups:the control group,the chitinase group,the HCC group,and the HCC+chitinase group.The antiproliferative effect of chitinase was evaluated in human HCC cells.The effect of chitinase in vivo on oxidative stress,endoplasmic reticulum stress chaperones,autophagy markers,PI3K/AKT/mTOR,AMPK pathway expression,and apoptotic indicators was determined and confirmed by histological examination.Results:Chitinase significantly inhibited the viabilities of HepG2 cells.Moreover,in the Wistar male rat model of HCC,chitinase decreased ATP levels,modulated endoplasmic reticulum stress,mediated autophagy factors,and promoted apoptosis.Conclusions:Chitinase might play a role in the apoptosis as well as autophagy pathways and may act as a potential tumor suppressor.
基金supported[in part]by the IntramuralResearch Program of the National Institutes ofHealth(NIH)(to KJM),and also supported by theOffice by the Office of the Assistant Secretary ofDefense for Health Affairs and the Defense HealthAgency J9,Research and Development Directorate,through the Vision Research Program under AwardNo.(CDMRPL-18-0-VR180205 to KJM and FMN-N).
文摘In vivo imaging of neurodegenerative diseases provides valuable insights into disease mechanisms and potential therapeutic interventions.Many ocular diseases are closely linked to neurodegenerative conditions affecting the brain,making the eye a unique and accessible model for studying these disorders.The transparency of eyes allows researchers to monitor disease progression non-invasively,offering a window into neural health.
文摘Oncology Research Editorial Office Published:19 January 2026 The published article titled“miR-126-5p Restoration Promotes Cell Apoptosis in Cervical Cancer by Targeting Bcl2l2”has been retracted from Oncology Research,Vol.25,No.4,2017,pp.463-470.DOI:10.3727/096504016X14685034103879 URL:https://www.techscience.com/or/v25n4/56826.
基金supported by the National Natural Science Foundation of China(Nos.82573045,82460602,82560459)the Hainan Provincial Graduate Student Innovative Research Project(No.Qhys2024-440).
文摘Post-translational modifications(PTMs)regulate the occurrence and development of cancer,and lactylation modification is a new form of PTMs.Recent studies have found that lactic acid modification can regulate the immune tolerance of cancer cells.The classical theory holds that prostate apoptosis response-4(PAR-4)is a tumor suppressor protein.However,our recent research has found that PAR-4 has a biological function of promoting cancer in hepatocellular carcinoma(HCC),and our analysis shows that PAR-4 can be modified of lactic acid.These research evidences suggest that PAR-4 lactylation modification may drive immune tolerance in HCC.Therefore,inhibiting PAR-4 lactylation modification is very likely to increase the sensitivity of HCC to immunotherapy.
基金supported by an NIH grant R01 DE031413 (M.V.B.)。
文摘Temporomandibular joint osteoarthritis(TMJ-OA) affects a significant proportion of the population worldwide.However,there has been no substantial progress in the development of FDA-approved drugs for treatment due to a lack of understanding of the specific factors regulating key TMJ-OA molecular mechanisms.Lysyl Oxidase-Like-2(LOXL2) promotes knee joint cartilage protection and is down regulated in a TMJ-OA animal model.We evaluated the role of LOXL2 in TMJ cartilage,its molecular mechanism,and gene networks using in vivo Loxl2 knockout mice(Acan-Cre;Loxl2^(flox/flox)) and ex vivo goat TMJ cartilage.Our results show that Loxl2 knockout in mouse cartilage upregulates Il1b,Mmp9,Mmp13,Adamts4,and Adamts5,but reduces the levels of aggrecan and proteoglycan.Loxl2 deleted TMJ cartilage show a higher enrichment of inflammatory response,TNFA signaling via NF-κB,extracellular matrix(ECM),and collagen degradation pathway network.Conversely,LOXL2 treatment reduces interleukin-1beta(IL-1β)-induced expression of Mmp13,protects mitochondrial function,and ECM from degeneration.Importantly,LOXL2attenuates IL-1 β-induced chondrocyte apoptosis via the phosphorylation of NF-κB and expression of the pain-related gene PTGS2(encodes COX2).Taken together,Loxl2 knockout mice exacerbate TMJ-OA through cartilage/ECM degradation,mitochondrial dysfunction,chondrocyte apoptosis,and inflammatory gene expression,whereas LOXL2 treatment mitigate these effects.
基金supported by the Major Science and Technology Project of Hubei Province(2020ACA007)the Scientific and Technological Bureau of Wuhan(2018060401011308).
文摘Nekemias megalophylla is a popular folk tea consumed by people in the Western Hubei(China)of which ampelopsin(AMP)is the main active ingredient.In this study,we investigated the effect of AMP on cervical cancer and explored its mechanism of action,focusing on apoptosis and autophagy.Firstly,we verified that AMP strongly inhibited the growth of C-33A cells and observed apoptosis and autophagy phenomenon in vivo,and found that AMP induces C-33A cell apoptosis via death receptor or mitochondrial pathways.The results also indicated that AMP-induced autophagy occurs via the PI3K/Akt/m TOR pathway.Secondly,when autophagy was inhibited,the AMP-induced apoptosis of C-33A cells was strengthened,when apoptosis was inhibited,the AMP-induced autophagy of C-33A cells was strengthened.PI3K/Akt/m TOR pathway activation enhances AMP-induced apoptosis in C-33A cells,while its inhibition strengthens AMP-induced autophagy.Finally,we confirmed that AMP inhibited cell growth and induced apoptosis and autophagy of C-33A cells in an in vivo nude mouse model of C-33A tumor xenografts.These results elucidate that AMP bidirectionally regulates apoptosis and autophagy in human cervical cancer C-33A cells by mediating the PI3K/Akt/m TOR pathway.
文摘Crosstalk between the nervous system and cancer plays an important role in tumor metastasis yet is poorly understood.Recently,Padmanaban et al.demonstrated a novel mechanism for nerve-induced metastasis.Sensory nerve-derived substance P could induce apoptosis in breast cancer cells that overexpressed tachykinin receptors.Single-stranded RNAs(ssRNAs)leaking from dying cells subsequently interact with toll-like receptor 7(TLR7)on other cancer cells and finally promoted metastasis.This notable study displays a delicate loop between the nervous system and cancer and,more importantly,amplifies the conception of apoptosis-induced metastasis.Over the past years,a mass of breakthrough studies have proven the pivotal role of the nervous system in tumorigenesis and cancer progression thereby contributing to the creation of a new disciplinecancer neuroscience[1].Hanahan and Monje discussed in detail the interactions between the nervous system and tumors based on the theoretical framework of the cancer hallmarks,focused on nerve-mediated proliferation,angiogenesis,immune evasion,cell death resistance,and metastasis[2].
文摘The published article titled“MicroRNA-98-5p Inhibits Cell Proliferation and Induces Cell Apoptosis in Hepatocellular Carcinoma via Targeting IGF2BP1”has been retracted from Oncology Research,Vol.25,No.7,2017,pp.1117–1127.
基金Jiangxi Provincial Department of Education Science and Technology Project(Grant No.GJJ2401615)Jiangxi Provincial Department of Education Teaching Reform Project(Grant No.JXJG-24-15-15).
文摘The aim of this study is to investigate the mechanism of magnesium isoglycyrrhizinate(MgIG)in the treatment of myocardial remodeling induced by isoproterenol(ISO)in mice.We assessed the impact of MgIG on ISO-induced myocardial remodeling by activating the PI3K/AKT1 pathway.The cardiac function of mice was evaluated by echocardiography,revealing that MgIG could improve left ventricular function.Pathological staining analysis showed that MgIG could reduce the degree of myocardial injury caused by ISO.Serum data detected by ELISA demonstrated that MgIG could decrease the levels of CK-MB,MDA,and LDH while increasing the activity of GSH-Px.Western blotting analysis revealed that protein expression levels of Collagen I,BNP,Bax,cleaved caspase-3,p-PI3K,and p-AKT1 were decreased,whereas the protein expressions of Bcl-2,COX2,and SOD1 were increased upon MgIG treatment.However,the activation of the PI3K pathway reversed the cardioprotective effects of MgIG,as evidenced by the addition of PI3K activators.Taken together,our comprehensive results suggested that MgIG could improve ISO-induced myocardial remodeling,potentially through its mechanism of inhibiting the PI3K/AKT1 pathway to regulate apoptosis and oxidative stress.
基金supported by CACMS Innovation Fund(No CI2021A04611,CI2021A05106)Scientific and technological innovation project of China Academy of Chinese Medical Sciences(CI2021B015)+1 种基金Scientific and technological innovation project of China Academy of Chinese Medical Sciences(CI2023E001TS01)Fundamental research funds for the central public welfare research institutes(L2022035).
文摘Objective Emerging evidence suggests that exposure to ultrafine particulate matter(UPM,aerodynamic diameter<0.1μm)is associated with adverse cardiovascular events.Previous studies have found that Shenlian(SL)extract possesses anti-inflammatory and antiapoptotic properties and has a promising protective effect at all stages of the atherosclerotic disease process.In this study,we aimed to investigated whether SL improves UPM-aggravated myocardial ischemic injury by inhibiting inflammation and cell apoptosis.Methods We established a mouse model of MI+UPM.Echocardiographic measurement,measurement of myocardialinfarct size,biochemical analysis,enzyme-linked immunosorbent assay(ELISA),histopathological analysis,Transferase dUTP Nick End Labeling(TUNEL),Western blotting(WB),Polymerase Chain Reaction(PCR)and so on were used to explore the anti-inflammatory and antiapoptotic effects of SL in vivo and in vitro.Results SL treatment can attenuate UPM-induced cardiac dysfunction by improving left ventricular ejection fraction,fractional shortening,and decreasing cardiac infarction area.SL significantly reduced the levels of myocardial enzymes and attenuated UPM-induced morphological alterations.Moreover,SL significantly reduced expression levels of the inflammatory cytokines IL-6,TNF-α,and MCP-1.UPM further increased the infiltration of macrophages in myocardial tissue,whereas SL intervention reversed this phenomenon.UPM also triggered myocardial apoptosis,which was markedly attenuated by SL treatment.The results of in vitro experiments revealed that SL prevented cell damage caused by exposure to UPM combined with hypoxia by reducing the expression of the inflammatory factor NF-κB and inhibiting apoptosis in H9c2 cells.Conclusion Overall,both in vivo and in vitro experiments demonstrated that SL attenuated UPMaggravated myocardial ischemic injury by inhibiting inflammation and cell apoptosis.The mechanisms were related to the downregulation of macrophages infiltrating heart tissues.
基金Supported by Science and Technology Research Program of Jilin Provincial Department of Education,No.JJKH20231218KJProject of the Jilin Provincial Administration of Traditional Chinese Medicine,No.2024111.
文摘Diabetic kidney disease(DKD)has a high incidence and mortality rate and lacks effective preventive and therapeutic methods.Apoptosis is one of the main reasons for the occurrence and development of DKD.Mesenchymal stem cells(MSCs)have shown great promise in tissue regeneration for DKD treatment and have protective effects against DKD,including decreased blood glucose and urinary protein levels and improved renal function.MSCs can directly differ-entiate into kidney cells or act via paracrine mechanisms to reduce apoptosis in DKD by modulating signaling pathways.MSC-derived extracellular vesicles(MSC-EVs)mitigate apoptosis and DKD-related symptoms by transferring miRNAs to target cells or organs.However,studies on the regulatory mechanisms of MSCs and MSC-EVs in apoptosis in DKD are insufficient.This review compre-hensively examines the mechanisms of apoptosis in DKD and research progress regarding the roles of MSCs and MSC-EVs in the disease process.
基金supported by China Agriculture Research System of MOF and MARA(CARS-40)the National Natural Science Foundation of China(32302776)。
文摘Background Higher embryonic mortality,especially in aged breeding hens,is associated with insufficient hepatic functionality in maintaining redox homeostasis.Our previous study demonstrated that egg exosome-derived miRNAs may play a key role in modulating embryonic oxidation-reduction process,whereas the exact function and mechanism were still poorly understood.The present study aimed to investigate the roles of egg exosome miRNAs in maintaining dynamic equilibrium of free radicals and peroxide agents in embryonic liver,as well as demonstrate the specific mechanism using oxidative stress-challenged hepatocytes.Results Compared to 36-week-old breeding hens,decreased hatchability and increased embryonic mortality were observed in 65-week-old breeding hens.Meanwhile,the older group showed the increased MDA levels and decreased SOD and GSH-Px activities in embryonic liver,muscle and serum.Embryonic mortality was significantly positively correlated with MDA level and negatively correlated with GSH-Px activity in embryonic liver.In addition,363 differentially expressed genes(DEGs)were identified in embryonic liver,13 differentially expressed miRNAs(DE-miRNAs)were identified in egg exosomes.These DEGs and DE-miRNAs were involved in oxidoreductase activity,glutathione metabolic process,MAPK signaling pathway,apoptosis and autophagy.miRNA-mRNA network analysis further found that DEGs targeted by DE-miRNAs were mainly enriched in programmed cell death,such as apoptosis and autophagy.Wherein,MAPK10 with highest MCC and AUC values was significantly related to GSH-Px activity and MDA level,and served as the target gene of miR-145-5p based on dual luciferase reporter experiment and correlation analysis.Bioinformatics analysis found that miR-145-5p/MAPK10 axis might alleviate peroxide generation and apoptosis.In primary hepatocytes of chick embryos,miR-145-5p transfection significantly reversed H_(2)O_(2)-induced mitochondrial ROS increase,MAPK10,BAX and CASP3 overexpression and excessive apoptosis.Conclusion Exosome miR-145-5p in eggs could target MAPK10 and decrease mitochondrial ROS,attenuating oxidative damage and apoptosis in hepatocytes of chick embryos.These findings may provide new theoretical basis for the improvement of maternal physiological status to maintain embryonic redox homeostasis by nutritional or genetic modifications.
基金supported by The National Natural Science Foundation of China(No.31902283)Research Foundation for Master students at the Affiliated Hospital of Zunyi Medical College(No.22-2018).
文摘Background:The outcomes of pediatric patients with acute lymphoblastic leukemia(ALL)remain far less than favorable.While apigenin is an anti-cancer agent,studies on the mechanism by which it regulates ALL cell cycle progression are inadequate.Ferroptosis and AMP-activated protein kinase(AMPK)signaling are important processes for ALL patients.However,it remains unclear whether apigenin works by affecting AMPK and apoptosis.Materials and Methods:SUP-B15 and T-cell Jurkat ALL cells were treated with apigenin,and cell viability and apoptosis were measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)and terminal deoxynucleotidyl transferase dUTP nick end labeling(TUNEL)assays,respectively.The thiobarbituric acid-reactive substances(TBARS)assay was used to evaluate lipid peroxidation.Intracellular Fe2+levels were measured using a commercial kit.Corresponding proteins were detected by western blotting.Results:Results showed that apigenin reduced cell viability and the levels of Ki67 and proliferating cell nuclear antigen(PCNA)expression in a concentration-dependent manner in both types of ALL cells.Apigenin also exerted anti-apoptotic effects on SUP-B15 and Jurkat cells.Apigenin activated AMP-activated protein kinase(AMPK)signaling and induced ferroptosis,and those effects were attenuated by inhibition of AMPK.Eventually,the reduced cell proliferation and increased cell apoptosis caused by apigenin in ALL cells were partly abolished by AMPK inhibition.Conclusion:In summary,apigenin exerted anti-leukemia activity in ALL cells,and that effect was partially achieved by activation of AMPK signaling.Our findings suggest apigenin as a potential drug for treatment of ALL.
基金National Key Research and Development Plan:Evidence-Based Evaluation and Therapeutic Mechanism Cooperation Study of Yishen Tongluo Formula for Preventing Diabetes Kidney Disease(Phase 3)(No.2020YFE0201800)Key Science and Technology Projects of Henan Province:Research on Innovative Drug Cooperation of Traditional Chinese Medicine Yishen Tongluo Concentrated Pills(益肾通络浓缩丸)(No.221111520300)+1 种基金Key scientific and technological projects of Henan province:Study on the Pharmacodynamic Mechanism of Yishen Tongluo Formula in Treatment of Diabetes Kidney Disease based on the Interaction Regulation of Protein Phosphorylation and Acylation Modification(No.212102310347)to WU SuhuiNational Natural Science Foundation of China:the Mechanism of Yishen Tongluo Formula Intervention in Diabetic Kidney Disease based on(Yin-Yang-1/Nuclear Factor Erythroid 2-Related Factor 2 Mediated Endothelial Podocyte Interaction Response(No.82474495)to XU Jiangyan。
文摘OBJECTIVE:To investigate the effect and mechanism of Yishen Tongluo formula(益肾通络方,YSTLF)in streptozotocin-induced diabetic kidney disease mice(DKD)mice.METHODS:Thirty Institute of Cancer Research mice(specific pathogen free,SPF grade)were divided into five groups(n=6 per group):control,DKD model,DKD model with YSTLF(4.9 g/kg),DKD model with YSTLF(9.8 g/kg),and DKD model with captopril.DKD was induced through a single intraperitoneal injection of streptozotocin(150 mg/kg).Body weight,fasting blood glucose and urine C-peptide levels were measured to assess metabolic regulation by YSTLF.Renal function was evaluated using indicators of glomerular and tubular health.Liver function was assessed by measuring aspartate aminotransferase and alanine aminotransferase levels.Renal pathological changes were examined using hematoxylin/eosin staining and transmission electron microscopy.Inflammatory and apoptosis-related factors were analyzed through enzyme-linked immunosorbent assay,immunohistochemistry,and Western blot analysis.RESULTS:In DKD mice,fasting blood glucose,Cpeptide,24-hour urine protein(UP)levels,and renal damage were elevated,accompanied by increased inflammation and apoptosis.YSTLF significantly reduced 24-hour UP and C-peptide levels and improved kidney and liver function in DKD mice.YSTLF also mitigated glomerular hypertrophy,basement membrane thickening,and podocyte foot process effacement.It upregulated the expression of the podocyte marker podocalyxin.Furthermore,YSTLF alleviated inflammation and apoptosis,likely by reducing the overexpression of monocyte chemoattractant protein(MCP-1),Bax,and Caspase-3 in the kidneys of DKD mice.CONCLUSIONS:These findings suggest that YSTLF ameliorates kidney injury by modulating the expression of inflammatory cytokine MCP-1 and the Bax/Caspase-3 apoptosis pathway,providing a potential therapeutic approach for DKD.
文摘Myocardial ischemia(MI)is a pathophysiological condition in which the myocardium is unable to maintain normal cardiac function due to insufficient coronary artery blood and oxygen supply,as well as abnormal myocardial energy metabolism[1].Ginsenoside Rbi(Rbi),one of the most abundant natural ingredients in ginseng and Panax notoginseng,has been proven to protect the heart from MI/reperfusion injury(RI)[2].
基金supported by grants from the National Natural Science Foundation of China(32170937)Shenzhen Medical Research Fund(SMRF,A2303015)+3 种基金Pearl River Talent Project of Guangdong Province(2021QN02Y426)Shenzhen Peacock Plan Project(827/000655)to Liang Yethe Yunnan Provincial Key Areas Science and Technology Plan Project(202303AC100025)Yunnan Scholar of Yunling(YNWRYLXZ-2019-019)to Rongping Zhang.
文摘Artemisia annua L.is a medicinal herb with multiple therapeutic applications,whereas its antiinfluenza A virus(IAV)efficiency and mechanism of action are still unclear.Here,we investigated the inhibition activity and mechanism of A.annua leaf methanol extracts(AALME)against IAV in vitro and in vivo.Our results revealed that AALME exhibits potent anti-IAV activity by interacting with IAV particles.Mechanistically,AALME directly targets the IAV nucleoprotein(NP)protein and abolishes the nuclear import of IAV NP.AALME profoundly suppresses IAV-induced mitochondrial apoptosis via suppressing ROS-mediated AIF-dependent pathways.More importantly,we found that AALME plays a crucial role in protecting mice from IAV infection and mitigating IAV pathogenicity.This current work provides mechanistic insight into the mechanism by which AALME controls IAV infection in vitro and in vivo,potentially contributing to the development of antiviral treatments for IAV infection.
