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ICAM2 loss drives 5-fluorouracil resistance via TGF-β/Smad/SP1/PTN-dependent apoptosis evasion and macrophage remodeling in gastric cancer 认领 引用 被引量：1
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作者 Xiao-Cheng Tang Zi-Jian Chen +6 位作者 Chun-Yu Chen Jun Qiu Jin-Tuan Huang Rong-Chang Tan Wei-Yao Li Hao Chen Zu-Li Yang 《World Journal of Gastroenterology》 SCIE CAS 2026年第5期125-147,共23页
BACKGROUND Chemoresistance significantly limits the therapeutic efficacy of neoadjuvant chemotherapy(NACT)in advanced gastric cancer(AGC).There is an urgent need to identify robust biomarkers predictive of NACT respon... BACKGROUND Chemoresistance significantly limits the therapeutic efficacy of neoadjuvant chemotherapy(NACT)in advanced gastric cancer(AGC).There is an urgent need to identify robust biomarkers predictive of NACT response and to elucidate the molecular mechanisms that drive resistance.In this study,we systematically assess whether intercellular adhesion molecule 2(ICAM2)predicts NACT response in patients with AGC and delineate its mechanistic role in chemoresistance.AIM To investigate the predictive significance and mechanistic role of ICAM2 in mediating 5-fluorouracil(5-FU)resistance in gastric cancer(GC).METHODS Real-time PCR,Western blotting,enzyme-linked immunosorbent assay,and immunohistochemistry were conducted to assess alterations in ICAM2 expression between 5-FU-sensitive and-resistant GC cells as well as in AGC patient samples.Cytotoxicity assays,colony formation,flow cytometry,analyses of apoptosis-related proteins,and xenograft experiments were employed to elucidate the role of ICAM2 in mediating chemoresistance.The mechanism underlying ICAM2-mediated chemoresistance was further explored through RNA sequencing(RNA-seq),nuclear-cytosolic fractionation,co-immunoprecipitation,luciferase reporter,and chromatin immunoprecipitation assays.RESULTS Low ICAM2 expression correlated significantly with poor NACT response,advanced tumor stage,worse differentiation,and reduced overall survival and disease-free survival in AGC patients.Pre-NACT serum ICAM2 demonstrated high predictive accuracy(area under the curve=0.876)in discriminating chemotherapy responders from non-responders.Mechanistically,ICAM2 knockdown conferred 5-FU resistance through two intertwined processes:Inhibition of caspase-dependent apoptosis and promotion of immunosuppressive M2 macrophage polarization within the tumor microenvironment.At the molecular level,loss of ICAM2 activated the TGF-β/Smad pathway,leading to transcription factor SP1-mediated pleiotrophin(PTN)upregulation.Elevated PTN further enhanced GC cell survival and may contribute to M2 macrophage polarization,thereby amplifying chemoresistance.Importantly,targeted inhibition of TGF-βsignaling reversed ICAM2-associated chemoresistance in both cell culture and xenograft models.CONCLUSION Our study highlights the clinical impact of ICAM2 downregulation predicting poor outcome and NACT response in AGC patients,and reveals a novel ICAM2/TGF-β/Smad/SP1/PTN signaling mediating 5-FU resistance in GC. 展开更多
关键词 Biomarker Chemoresistance Apoptosis Intercellular adhesion molecule 2 Tumor microenvironment Gastric cancer
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Schisandrin A ameliorates endoplasmic reticulum stress mediated apoptosis in metabolic associated fatty liver disease 认领 引用 被引量：1
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作者 Jing Zhou Ying Shi +8 位作者 Zuzhen Bao Mengmeng Luo Jie Li Marwan M.A.Rashed Suowen Xu Jianhua Yang Hong Duan Henggui Hu Kefeng Zhai 《Food Science and Human Wellness》 SCIE CAS CSCD 2026年第5期2093-2103,共11页
Metabolic associated fatty liver disease(MAFLD)is closely linked to metabolic disorders and lack of effective therapeutic options.Schisandrin A(SA),derived from the traditional Chinese medicinal herb Schisandra,has sh... Metabolic associated fatty liver disease(MAFLD)is closely linked to metabolic disorders and lack of effective therapeutic options.Schisandrin A(SA),derived from the traditional Chinese medicinal herb Schisandra,has shown liver-protective properties.SA may counteract MAFLD by modulating endoplasmic reticulum stress(ERS)and inhibiting apoptosis.This study aimed to investigate the protective effects of SA on high-fat diet-induced MAFLD in C57BL/6 mice.The study also sought to elucidate the underlying mechanisms,focusing on the ERS signaling pathway and apoptosis.A MAFLD mouse model was established by feeding mice a high-fat diet.The mice were then randomly divided into the following groups:control,model,SA intervention(various dosages),atorvastatin-treated positive control,and ERS inhibitor combined with SA intervention.Serum lipid profiles,liver enzymes,and liver histopathology were assessed.Western blot,immunofluorescence(IF),and TUNEL assay were used to evaluate ERS and apoptosis-related protein expression.SA intervention markedly enhanced serum lipid profiles and reduced liver enzyme levels.The histopathological alterations observed in the model group were significantly mitigated by SA treatment.Western blot analysis revealed that SA effectively modulated the expression levels of proteins associated with ERS and apoptosis.Furthermore,IF and TUNEL assay results substantiated SA's regulatory influence on ERS and apoptotic pathways.SA effectively improved dyslipidemia and hepatic lipid metabolism abnormalities.It reduced hepatic lipid deposition and pathological damage in MAFLD mice induced by a high-fat diet.The mechanism of action may involve the regulation of the ERS signaling pathway,thereby protecting cells from apoptosis. 展开更多
关键词 Metabolic associated fatty liver disease Schisandrin A Endoplasmic reticulum stress Apoptosis
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Environmentally relevant concentration of abamectin induces cardiac dysfunction in largemouth bass(Micropterus salmoides):Mechanistic insights into apoptosis,bioaccumulation and potential modulation 认领 引用
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作者 Rabia Tahir Kaige Song +8 位作者 Weizhe Luo Abhimanyu Shrestha Guojun Hu Zihan Huang Yifan Hu Han Yan Qiao Liu Liulan Zhao Song Yang 《Journal of Environmental Sciences》 SCIE EI CAS CSCD 2026年第6期849-862,共14页
The increasing contamination of aquatic ecosystems by agrochemicals and pharmaceuticals,such as abamectin(ABA),poses significant risks to fish and human health through bioaccumulation.Thereby,in the current study,larg... The increasing contamination of aquatic ecosystems by agrochemicals and pharmaceuticals,such as abamectin(ABA),poses significant risks to fish and human health through bioaccumulation.Thereby,in the current study,largemouth bass(Micropterus salmoides)were chronically exposed to 0.012 mg/L of ABA for six weeks.Concurrently,dietary supplementation with curcumin(CUR)at 50,100,and 200 mg/kg was administered to evaluate its protective effects against ABA-induced toxicity.ABA significantly decreased growth performance,while inducing severe behavioral alterations and cardiac damage,including necrosis,hemorrhage,and inflammatory infiltration.It triggered oxidative stress by decreasing antioxidants(superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),catalase(CAT),increasing inducible nitric oxide synthase(iNOS)and malondialdehyde(MDA),and disruption of nrf2,keap 1,ho-1,and nqo1.ABA-induced immune dysfunction and inflammation which were linked to NLRP3 inflammasome stimulation,demonstrated as enhanced alkaline phosphatase(AKP),acid phosphatase(ACP)and altered transcription and translation of il-10,il-1β,tgf-β1,tnf-α,asc,caspase1,nlrp3,and nf-κb.It caused apoptosis by dysregulating gene and protein level of fas,p53,bcl2,bax,and caspases.It disrupted autophagic flux by inhibiting mTOR signaling,resulting in increased expression of lc3ii,p62 and atg5;and decreased akt and mtor level.ABA residues were detected in heart tissues(P<0.01),and total hazard quotient(THQ)indicated potential human health risks due to bioaccumulation.Integrated biomarker response(IBR)analysis and molecular docking further confirmed the exposure risk of ABA.However,CUR co-treatment effectively attenuated these toxic effects and molecular interactions.Collectively,it highlighted the possible risks for human health,emphasizing its toxicological impact whereas protective role of CUR in mitigating ABA-induced cardiotoxicity suggests a promising strategy for reducing pesticide-related health hazards in aquaculture and environmental toxicology. 展开更多
关键词 Ecotoxicology Inflammation Apoptosis Immunity disruption Avermectins Curcumin
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ZBP1 promotes RIPK1-dependent apoptosis in aristolochic acid nephropathy 认领 引用
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作者 Zhenhuan Zou Keng Ye +7 位作者 Fengbin Chen Kongwen Lin Yankun Song Guoping Li Caiming Chen Yujia Wang Huabin Ma Yanfang Xu 《Zoological Research》 SCIE CSCD 2026年第2期577-592,共16页
Aristolochic acid nephropathy(AAN)is a progressive kidney disease marked by acute tubular injury and interstitial fibrosis that frequently advances to end-stage renal disease(ESRD).Despite regulatory restrictions,aris... Aristolochic acid nephropathy(AAN)is a progressive kidney disease marked by acute tubular injury and interstitial fibrosis that frequently advances to end-stage renal disease(ESRD).Despite regulatory restrictions,aristolochic acid(AA)continues to pose a global health risk due to persistent exposure through traditional herbal medicines.Although mitochondria-mediated apoptosis is a defining hallmark of AA-induced tubular epithelial cell(TEC)injury,the upstream molecular mechanisms remain poorly resolved.The present study identified Z-DNAbinding protein 1(ZBP1)as a key mediator of AAI-induced kidney injury.Using Zbp1 knockout(Zbp1−/−)and Zαdomain-mutant(ZαMut)mice,loss of ZBP1 or disruption of Z-form nucleic acid sensing conferred marked protection against AAI-induced renal dysfunction,apoptosis,and inflammation.Mechanistic analyses showed that aristolochic acid I(AAI)triggered mitochondrial oxidative stress and promoted mitochondrial DNA(mtDNA)release,after which mtDNA adopted a Z-conformation recognized by ZBP1.ZBP1 engagement then promoted RHIMdependent association with RIPK1,leading to caspase-8 activation and apoptotic cell death.Notably,ZBP1-mediated cell death was abolished by RIPK1 kinase inhibition or mutation but remained unchanged after Ripk3 or Mlkl deletion,indicating a pathway distinct from RIPK3/MLKL-dependent necroptosis.These findings define a previously unrecognized ZBP1-RIPK1-caspase-8 signaling axis that drives non-canonical apoptosis in AAN and identify this pathway as a potential therapeutic target in nephrotoxin-induced kidney injury. 展开更多
关键词 Aristolochic acid nephropathy Apoptosis Mitochondria ZBP1 Z-DNA
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Sanguinarine triggers apoptosis and ferroptosis synchronously by directly binding BiP in lung squamous cell carcinoma 认领 引用
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作者 Weidan Tan Xinyu Wei +8 位作者 Changsheng Li Huilan Wei Fei Yu Xiaoju Shen Xiaoxiang Mo Meifen Wei Shangping Xing Zhuo Luo Jie Yang 《Chinese Journal of Natural Medicines》 SCIE CAS CSCD 2026年第4期427-439,共13页
Lung squamous cell carcinoma(LUSC) is a prevalent and aggressive form of lung cancer with limited therapeutic options. Sanguinarine(SAG),a prominent benzophenanthridine alkaloid derived from Zanthoxylum nitidum(Roxb.)... Lung squamous cell carcinoma(LUSC) is a prevalent and aggressive form of lung cancer with limited therapeutic options. Sanguinarine(SAG),a prominent benzophenanthridine alkaloid derived from Zanthoxylum nitidum(Roxb.) DC,exhibits established anti-tumor activity;however,its molecular mechanisms in LUSC remain incompletely defined. In this study,the anti-cancer effects and underlying mechanisms of SAG were systematically investigated in vitro and in vivo. Cell viability and death were evaluated using methyl thiazolyl tetrazolium(MTT) assays,colony formation assays,flow cytometry,transmission electron microscopy(TEM),and Western blotting(WB). Drug affinity responsive target stability(DARTS) combined with liquid chromatography–tandem mass spectrometry(LC-MS/MS),molecular docking,cellular thermal shift assay(CETSA),and surface plasmon resonance(SPR) were employed to identify and validate molecular targets of SAG. The results demonstrated that SAG simultaneously induces apoptosis and ferroptosis in LUSC cells by directly targeting the endoplasmic reticulum(ER) chaperone binding immunoglobulin protein(Bi P). Silencing of Bi P markedly attenuated SAG-induced apoptosis and ferroptosis,confirming its essential role in this process. Mechanistically,SAG up-regulates Bi P expression and activates the protein kinase R-like endoplasmic reticulum kinase(PERK)/e IF2α/C/EBP homologous protein(CHOP)/GADD34 signaling axis of ER stress(ERS),ultimately leading to dual induction of apoptosis and ferroptosis in vitro and in vivo. 展开更多
关键词 Lung squamous cell carcinoma Sanguinarine Apoptosis Ferroptosis BiP
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Semaglutide ameliorates coronary microembolization-induced injury by suppressing apoptosis and inflammation via the HMGB1/RAGE/NF-κB p65 pathway 认领 引用
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作者 Hua-Feng YANG Hong-Qing LI +2 位作者 Qiang WANG Xian-Tao WANG Lang LI 《Journal of Geriatric Cardiology》 SCIE CAS CSCD 2026年第2期83-99,共17页
BACKGROUND Coronary microembolization(CME)is the major leading cause of perioperative myocardial injury during coronary revascularization.Semaglutide exerts multiple protective biological activities,but its cardioprot... BACKGROUND Coronary microembolization(CME)is the major leading cause of perioperative myocardial injury during coronary revascularization.Semaglutide exerts multiple protective biological activities,but its cardioprotective effects on CME remain unclear.Thus,this experiment studied the impact of semaglutide on CME-induced myocardial injury.METHODS A rat CME model was generated by injecting microspheres into the left ventricle while clamping the ascending aorta.A H9c2 cardiomyocyte model was constructed by stimulation of lipopolysaccharide combined with hypoxia.Semaglutide or the high mobility group box 1(HMGB1)antagonist glycyrrhizin administrations were ahead of CME and cell modeling.Cardiac function,myocardial injury markers,cell viability and morphological alternations were detected.Apoptotic and inflammatory factors,cytosolic HMGB1 and its translocation,advanced glycosylation end-product specific receptor(RAGE),and nuclear factor kappa B p65(NF-κB p65)were evaluated.RESULTS Semaglutide pretreatment ameliorated CME-induced cardiac systolic dysfunction and relieved the cardiac injury.Semaglutide attenuated myocardial apoptosis and inflammatory response following CME in vivo and in vitro.Moreover,semaglutide downregulated HMGB1 expression and suppressed its nuclear-cytoplasmic translocation.Both glycyrrhizin and semaglutide administration affected the HMGB1/RAGE/NF-κB p65 pathway after CME.CONCLUSIONS Semaglutide pretreatment attenuates CME-induced myocardial injury by suppressing apoptosis and inflammation through the HMGB1/RAGE/NF-κB p65 pathway. 展开更多
关键词 injecting microspheres semaglutide inflammation h c cardiomyocyte model myocardial injury coronary microembolization apoptosis coronary revascularizationsemaglutide
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Piericidin F,a Novel Marine-Derived Piericidin Derivative,Degrades High-Risk HPV Oncoproteins E6/E7 by ROS-Dependent Ubiquitin Proteasome System and Induces Apoptosis in HeLa Cells 认领 引用
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作者 ZHANG Weiyi CHEN Yifan +5 位作者 CHANG Yimin HAN Xiaoning YANG Yufeng GU Qianqun LI Dehai LIU Ming 《Journal of Ocean University of China》 SCIE CAS CSCD 2026年第3期1133-1142,共10页
High-risk human papillomavirus(HPV)oncoproteins E6/E7 are essential for cellular carcinogenesis and malignant growth in HPV-positive cervical cancers,and these oncoproteins have been considered as promising targets fo... High-risk human papillomavirus(HPV)oncoproteins E6/E7 are essential for cellular carcinogenesis and malignant growth in HPV-positive cervical cancers,and these oncoproteins have been considered as promising targets for cervical cancer treatment.Here,for the first time,we report that piericidin F(PdF),a new piericidin derivative derived from marine Streptomyces,inhibits cell proliferation and induces cell apoptosis in HPV-positive human cervical cancer HeLa cells.Molecular mechanism studies showed that PdF disrupted the mitochondria function and inhibited the function of mitochondrial respiration chains complex I.Subsequently,this increased generation of ROS stimulates oncoproteins E6/E7 degradation via ubiquitin proteasome system.In short,we reveal a new mechanism underlying the anti-cancer activity of piericidin compounds by disrupting mitochondrial function and degrading oncoproteins E6/E7 in HPV-positive cervical cancers,and highlight that PdF has the potential to be a lead compound for therapeutic agents against HPV-positive cervical cancers. 展开更多
关键词 piericidin derivative ubiquitin proteasome system apoptosis reactive oxygen species E6/E7 cervical cancer
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Benzofuran-isatin derivative 5d acts as a dual-action agent in colorectal cancer cells by targeting EMT and mitochondrial apoptosis pathways 认领 引用
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作者 Maha Hamadien Abdulla Mansoor-Ali Vaali-Mohammed +7 位作者 Sabine Matou Nasri Noura S.Alhassan M.Meeramaideen Abdullah Al Obeed Wagdy M.Eldehna Rofaida Salem Thamer Traiki Khayal Al Khayal 《Asian Pacific Journal of Tropical Biomedicine》 SCIE CAS 2026年第5期212-224,I0001,I0002,共13页
Objective:To investigate the anticancer effects of a novel benzofuran-isatin conjugate[N’-(5-methoxy-2-oxoindolin-3-ylidene)-3-methylbenzofuran-2-carbohydrazide(conjugate 5d)]against human colorectal adenocarcinoma(C... Objective:To investigate the anticancer effects of a novel benzofuran-isatin conjugate[N’-(5-methoxy-2-oxoindolin-3-ylidene)-3-methylbenzofuran-2-carbohydrazide(conjugate 5d)]against human colorectal adenocarcinoma(CRC)HT29 and metastatic SW620 colorectal cancer cells.Methods:The cytotoxic properties of conjugate 5d were evaluated using the MTT assay.Its anti-oncogenic effects were assessed by real-time monitoring of cell proliferation,migration,and invasion,and by performing a clonogenic assay.Flow cytometry was also used to assess the apoptotic status and cell cycle.Apoptosis,cell cycle,and epithelial-mesenchymal transition-related protein and gene expression levels were also measured.Results:Conjugate 5d exhibited cytotoxic effects on both CRC cells and enhanced the cytotoxic efficacy of 5-fluorouracil,irinotecan,and oxaliplatin.Conjugate 5d also induced apoptosis by modulation of anti-apoptotic(i.e.,Bcl-xl)and pro-apoptotic(i.e.,Bax,p53,cytochrome c)proteins,and MMP loss.Docking studies predicted molecular interactions of conjugate 5d with anti-apoptotic Bcl-2,revealing conjugate 5d as a potential Bcl-2 inhibitor.Regarding the oncogenic process,conjugate 5d inhibited CRC cell proliferation,migration,invasion,and colony formation,upregulated E-cadherin expression,and downregulated N-cadherin expression.Conclusions:Conjugate 5d shows significant anticancer effects against HT29 and SW620 cells by exerting pro-apoptotic and anti-metastatic activities.It also enhances the cytotoxic efficacy of conventional chemotherapeutic drugs in CRC cell lines.However,in vivo studies should be conducted to further confirm its efficacy. 展开更多
关键词 Colorectal cancer Synthetic benzofuran-isatin conjugate Apoptosis Cell cycle Anticancer Epithelial-mesenchymal transition
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Regulation of cancer cell apoptosis with DNA nanocalculator 认领 引用
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作者 Yongjian Jiang Feng Cheng +3 位作者 Jun Zhou Lei Zhan Chunmei Li Chengzhi Huang 《Chinese Chemical Letters》 SCIE CAS CSCD 2026年第1期507-513,共7页
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
关键词 Apoptosis DNA nanocalculator Logic gate Nucleolin Cytochrome c
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Mechanism of anti-human antigen D(HuD/ELAVL4)autoantibodyinduced enteric neuronal apoptosis in irritable bowel syndrome and its potential for targeted intervention 认领 引用
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作者 Yu Zhang Chen Zhu +7 位作者 Su-Hong Xia Ming-Yu Zhang Yi-Ran Liu Jia-Lun Guan Yu-Jie Huang Kai Zhao Jia-Zhi Liao Wen-Juan Fan 《World Journal of Gastroenterology》 SCIE CAS 2026年第22期68-87,共20页
BACKGROUND Irritable bowel syndrome(IBS)is a common disorder of gut-brain interaction and is characterized by chronic abdominal pain and altered bowel habits.Current evidence indicates that immune activation and autoa... BACKGROUND Irritable bowel syndrome(IBS)is a common disorder of gut-brain interaction and is characterized by chronic abdominal pain and altered bowel habits.Current evidence indicates that immune activation and autoantibody production contribute to IBS pathogenesis.However,the mechanisms by which autoantibodies affect the enteric nervous system and contribute to IBS-related symptoms are poorly understood.AIM To investigate the role of anti-human antigen D[HuD,also known as ELAV-like protein 4(ELAVL4)]autoantibodies in enteric neuronal apoptosis in an IBS animal model.METHODS A passive-transfer rat model of IBS was generated by intraperitoneal administration of HuD autoantibodies.Gastrointestinal motility,visceral sensitivity,fecal output,and water content were assessed.Enteric neuronal apoptosis in intestinal tissues and primary enteric neurons was analyzed by immunofluorescence.Mechanisms were examined using quantitative reverse transcription polymerase chain reaction,western blotting,and confocal microscopy.Interventions included recombinant HuD,immunoglobulin,5-hydroxytryptamine receptor modulators,and protein kinase C(PKC)agonists.RESULTS Administration of HuD autoantibodies induced IBS-like phenotypes in rats.We observed increased fecal output,elevated fecal water content,accelerated intestinal transit,and enhanced visceral hypersensitivity.HuD autoantibody exposure significantly increased enteric neuronal apoptosis in vivo and in vitro and suppressed the expression of special AT-rich sequence-binding protein 1(SATB1).Mechanistically,HuD autoantibodies disrupted HuD-mediated RNA regulation,leading to SATB1 downregulation and inhibition of the phosphatidylinositol 3-kinase(PI3K)-protein kinase B(AKT)signaling pathway.PKC activation restored HuD and SATB1 expression,reactivated PI3K-AKT signaling,and significantly reduced neuronal apoptosis.Treatment with immunoglobulin and 5-hydroxytryptamine receptor agonists showed limited or inconsistent protective effects.CONCLUSION HuD autoantibodies induced enteric neuronal apoptosis through disruption of the HuD-SATB1-PI3K-AKT signaling axis and contributed to IBS-like gastrointestinal dysfunction.Activation of PKC may be a potential therapeutic strategy for IBS. 展开更多
关键词 Irritable bowel syndrome Anti-HuD autoantibody Enteric neuron Apoptosis Intervention
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Chaihu-Shugan-San ameliorates chronic atrophic gastritis by inhibiting nuclear factor-kappa B-mediated inflammation and apoptosis 认领 引用
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作者 Jin Song Dan-Yan Li +6 位作者 Xiao-Li Zhang Sha-Sha He Ning Wang Hui-Cun Zhang Yun-Jing Bai Bo Li Sheng-Sheng Zhang 《World Journal of Gastroenterology》 SCIE CAS 2026年第10期134-151,共18页
BACKGROUND Chaihu-Shugan-San(CSS),a classic traditional Chinese medicine formula,has demonstrated significant efficacy in treating various gastrointestinal disorders.AIM To explore the therapeutic efficacy of CSS in a... BACKGROUND Chaihu-Shugan-San(CSS),a classic traditional Chinese medicine formula,has demonstrated significant efficacy in treating various gastrointestinal disorders.AIM To explore the therapeutic efficacy of CSS in alleviating chronic atrophic gastritis(CAG),and elucidate the underlying mechanisms of action.METHODS High performance liquid chromatography-mass spectrometry was used to identify the main active components of CSS.The therapeutic effects of CSS at doses of 925 mg/kg/day and 1850 mg/kg/day on N-methyl-N’-nitro-N-nitrosoguanidine(MNNG)-induced CAG were evaluated.Network pharmacology and molecular docking were used to predict the potential targets of CSS in CAG.The impact of CSS on the gut microbiota of rats was investigated by 16S rRNA sequencing.RESULTS The main active components of CSS were lipids and lipid-like molecules,phenylpropanoids and polyketides.In vivo experiments showed that CSS significantly ameliorated MNNG-induced CAG by inhibiting inflammation and apoptosis.The core target of CSS to alleviate CAG were tumor necrosis factor,interleukin(IL)-1β,IL-6,BAX,BCL2,caspase-3/caspase-9,and NFKBIA.Gene Ontology analysis of these core targets revealed their predominant association with the nuclear factor-kappa B(NF-κB)signaling complex and BAX apoptotic complex.Molecular docking demonstrated that six compounds in CSS,including baicalin,licoisoflavone B,licochalcone B,glabrone,glycyrrhiza flavonol A,and marmin exhibited strong binding affinities with NFKBIA.16S rRNA sequencing indicated that CSS promoted beneficial changes in the colonic microbial community.CONCLUSION CSS alleviated CAG by inhibiting NF-κB-mediated inflammation and apoptosis,providing insights into its mechanism of action in protection against CAG. 展开更多
关键词 Chronic atrophic gastritis Chaihu-Shugan-San Inflammation Apoptosis Nuclear factor-kappa B
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CDCA7 Promotes Proliferation and Suppresses Apoptosis in Gastric Cancer via HELLS-Mediated Chromatin Remodeling 认领 引用
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作者 Jun Jiang Yi-Ran Li +5 位作者 Xiaoting Wang Jian Li Fangzhou Ye Jiayi Wang Huanqing Li Li Feng 《Oncology Research》 SCIE 2026年第5期741-759,共19页
Background:In various tumor types,cell division cycle-associated 7(CDCA7)is involved in chromatin remodeling andDNA methylation.However,its biological functions and regulatorymechanisms in gastric cancer(GC)remain unk... Background:In various tumor types,cell division cycle-associated 7(CDCA7)is involved in chromatin remodeling andDNA methylation.However,its biological functions and regulatorymechanisms in gastric cancer(GC)remain unknown.This investigation intended to identify the function of CDCA7 in GC progression and elucidate its epigenetic regulatory mechanisms.Methods:Differentially expressed genes(DEGs)were detected fromthe GSE19826,TCGA-GC,and GSE56807 datasets.Networks of protein-protein interactions(PPI)and hub genes were discovered by the DMNC and Clustering Coefficient algorithms.Receiver operating characteristic(ROC)analysis and expression profiling were undertaken to determine diagnostic performance.In vitro assays,including CCK-8 assays,clonogenic assays,flow cytometry,dot blots,co-immunoprecipitation(Co-IP),chromatin immunoprecipitation(ChIP),and Western blots,were applied to evaluate the role of CDCA7 and its interaction with helicase,lymphoid-specific(HELLS).Results:169 overlapping genes were discovered,enriched in Cell adhesion molecules and ECM-receptor interaction.CDCA7 is highly expressed in GC and has high clinical diagnostic value.Knockdown of CDCA7 causes apoptosis and suppresses GC cell invasion,migration,and proliferation.Mechanistically,CDCA7 physically interacts with HELLS and promotes HELLS recruitment to chromatin.Knockdown of CDCA7 reduces global 5 hmC/5 mC levels and histone methylation(H3K9me3 and H4K20me3),while HELLS overexpression partially reverses these effects.Functionally,HELLS overexpression also partially reverses the antiproliferative and proapoptotic effects of CDCA7 knockdown.Conclusion:CDCA7 promotesGC progression by interactingwith HELLS to regulateDNAmethylation and chromatin stability,suggesting that the CDCA7-HELLS axis may serve as a potential diagnostic biomarker and therapeutic target for GC. 展开更多
关键词 CDCA7 HELLS chromatin remodeling gastric cancer proliferation apoptosis
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Bisphenol A-induced oxidative stress mediated by mitochondrial dysfunction triggers ferroptosis and apoptosis pathways in marine clams Meretrix petechialis 认领 引用
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作者 Xiaotian WANG Zhengjia WEI +4 位作者 Shangjie ZHOU Yan LIU Pengfei CHU Xinghong XU Long ZHU 《Journal of Oceanology and Limnology》 SCIE CAS CSCD 2026年第3期1159-1175,共17页
Bisphenol A(BPA)is a widely used chemical compound that has been shown to exert deleterious effects on living organisms.In aquatic species,the hepatopancreas,a key organ responsible for detoxification,is susceptible t... Bisphenol A(BPA)is a widely used chemical compound that has been shown to exert deleterious effects on living organisms.In aquatic species,the hepatopancreas,a key organ responsible for detoxification,is susceptible to damage,which can significantly impact the health and survival of these organisms.The effects of BPA on the hepatopancreas of Meretrix petechialis were investigated,for which M.petechialis were exposed to 0-,1-,10-,100-μg/L BPA for 14 d.Histopathological and ultrastructural analyses,including Hematoxylin and Eosin(H&E)staining and transmission electron microscopy(TEM),revealed that BPA exposure resulted in hepatopancreatic injury,mitochondrial damage,and an abnormal increase in autophagosomes.Transcriptome analysis further identified differentially expressed genes(DEGs)significantly associated with oxidative stress,apoptosis,and ferroptosis pathways.Following BPA exposure,levels of oxidative stress markers,such as hydrogen peroxide(H2O2),malondialdehyde(MDA),and superoxide dismutase(SOD)activity increased.In addition,ferroptosis-related indicators showed notable changes with increased tissue Fe2+ content and decreased glutathione peroxidase 4(GPX4)activity.The TUNEL assay also indicated an increased abundance of apoptotic cells.Finally,qRT-PCR was performed,confirming the dysregulation of genes involved in ferroptosis,apoptosis,and autophagy.This study demonstrated that BPA exposure induces oxidative stress in M.petechialis,leading to histopathological damage,mitochondrial dysfunction,and an abnormal accumulation of autophagosomes,ultimately triggering the activation of ferroptosis and apoptosis pathways.These findings advanced our understanding of the toxicity mechanisms of BPA in marine bivalves and facilitated the risk assessment of BPA in aquatic environments. 展开更多
关键词 bisphenol A(BPA) mitochondrial damage ferroptosis apoptosis Meretrix petechialis
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PI3K/Akt/mTOR-mediated bidirectional regulation of ampelopsin from Nekemias megalophylla modulates autophagy and apoptosis in cervical cancer 认领 引用
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作者 Shiyi Xu Siyu Liao +6 位作者 Juan Xi Ling Gong Xue Zou Xiaoli Yang Jiangxue Di Xiuqiao Zhang Chun Gui 《Food Science and Human Wellness》 SCIE CAS CSCD 2026年第2期804-822,共19页
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
关键词 Ampelopsin Apoptosis Autophagy C-33A cell PI3K/Akt/mTOR Bidirectional regulation
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Free fatty acids induce apoptosis in mammary epithelial cells from ketotic dairy cows via endoplasmic reticulum stress 认领 引用
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作者 Renxu Chang Yuanyuan Chen +7 位作者 Xinyi Xu Hongdou Jia John Mauck Juan J.Loor Yehoshav A.Ben Meir Qiushi Xu Xudong Sun Chuang Xu 《Journal of Integrative Agriculture》 SCIE CAS CSCD 2026年第5期2014-2027,共14页
The mammary glands of dairy cows with ketosis face unique challenges,including the supraphysiological circulating concentrations of free fatty acids(FFA) and apoptosis of epithelial cells.The fact that endoplasmic ret... The mammary glands of dairy cows with ketosis face unique challenges,including the supraphysiological circulating concentrations of free fatty acids(FFA) and apoptosis of epithelial cells.The fact that endoplasmic reticulum(ER) stress and apoptosis are closely related processes(at least in nonruminants) suggests that mechanisms of metabolic stressinduced apoptosis in bovine mammary epithelial cells may involve the ER stress pathway.The objective of this study was to investigate(1) the status of the ER stress pathway in mammary gland of dairy cows with ketosis,and(2) the role of ER stress in the apoptosis of bovine mammary epithelial cells challenged with high concentrations of FFA.Ketosis or exogenous FFA activated the ER stress pathway in the mammary gland of dairy cows or MAC-T cells.Pretreatment with the ER stress activator Tunicamycin(Tun) aggravated ER stress and apoptosis in MAC-T cells induced by FFA.However,ER stress inhibitor Tauroursodeoxycholate(TUDCA) attenuated ER stress induced by FFA and also attenuated the apoptosis in MAC-T cells.In conclusion,the data confirmed that FFA induced apoptosis of bovine mammary epithelial cells in dairy cows with ketosis via ER stress signaling.Thus,timely resolution of ER stress may help counteract the negative effects of ketosis on the mammary gland. 展开更多
关键词 ketosis bovine mammary epithelial cells ER stress apoptosis
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Correction to“Synergism of calycosin and bone marrow-derived mesenchymal stem cells to combat podocyte apoptosis to alleviate adriamycin-induced focal segmental glomerulosclerosis” 认领 引用
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作者 Qiong-Dan Hu Rui-Zhi Tan +4 位作者 Yuan-Xia Zou Jian-Chun Li Jun-Ming Fan Fahsai Kantawong Li Wang 《World Journal of Stem Cells》 SCIE 2026年第2期114-117,共4页
This is an erratum to the published paper entitled“Synergism of calycosin and bone marrow-derived mesenchymal stem cells to combat podocyte apoptosis to alleviate adriamycin-induced focal segmental glomerulosclerosis... This is an erratum to the published paper entitled“Synergism of calycosin and bone marrow-derived mesenchymal stem cells to combat podocyte apoptosis to alleviate adriamycin-induced focal segmental glomerulosclerosis”.Upon reexamining our original data,we have identified an error in the assembly of Figure 1F,where the glyceraldehyde-3-phosphate dehydrogenase loading control image was incorrectly placed due to a clerical oversight during figure preparation.This does not reflect any issue with the underlying experimental data. 展开更多
关键词 Correction Calycosin Mesenchymal stem cells Focal segmental glomerulosclerosis Apoptosis Smad3
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Plexin A2 Knockdown Enhances Apoptosis in Chemotherapy Treated Melanoma Cells 认领 引用
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作者 Nadezhda Palkina Aleksandra Esimbekova +6 位作者 Ekaterina Lapkina Victoriia Kutsenko Ivan Zinchenko Egor Dereviankin Elena Anisimova Andrei Savchenko Tatiana Ruksha 《Oncology Research》 SCIE 2026年第5期643-666,共24页
Background:Cancer cells are characterized by the ability to exit reversibly from the cell cycle to resist an unfavorable environment.This study elucidates alterations in adhesion molecule expression in melanoma cells ... Background:Cancer cells are characterized by the ability to exit reversibly from the cell cycle to resist an unfavorable environment.This study elucidates alterations in adhesion molecule expression in melanoma cells acquiring resistance to dacarbazine(DTIC)and entering the G0 state.Plexin A2(PLXNA2)was identified as a focal adhesion-related molecule implicated in carcinogenesis.Methods:Applying siRNA-mediated knockdown,the effects of altered PLXNA2 expression in melanoma cells were evaluated.PLXNA2 expression was determined by real-time quantitative reverse transcription PCR,immunoblotting,and immunocytochemistry.Cell cycle phase distribution among dacarbazine-treated cells and their apoptosis levels were quantified by flow cytometry,while adhesion to fibronectin was evaluated spectrophotometrically.Results:Our findings indicated that DTIC treatment modulates melanoma cell interactions with the extracellular matrix,facilitating adhesion to collagen IV,fibronectin,and laminin.Concurrently,integrin expression diminishes upon DTIC exposure.Delete Crucially,focal adhesion signaling molecules,including PLXNA2,Phosphoinositide-3-Kinase Regulatory Subunit 1,and Fibroblast Growth Factor Receptor 2,exhibit increased expression.PLXNA2 knockdown in DTIC-treated melanoma cells did not affect the percentage of cells residing in the G0 phase of the cell cycle.However,it induced apoptosis in DTIC-treated SK-MEL-2 and A375 melanoma cells and G1 cell cycle arrest in A375 melanoma cells.Conclusions:These findings suggest that PLXNA2 down-regulation in DTIC-treated cancer cells promotes their apoptosis.Therefore,targeting focal adhesion molecules during chemotherapy can increase the sensitivity of tumor cells to anticancer treatment. 展开更多
关键词 Apoptosis chemoresistance melanoma plexin A2(PLXNA2) quiescence
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2-Amino-3-methylimidazo[4,5-f]quinoline induces oxidative stress-mediated DNA damage and apoptosis in multi-organ of zebrafish 认领 引用
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作者 Dan Li Weiye Liu +5 位作者 Yu Jiang Xiang Gao Yingshuang Lu Yan Zhang Huan Lv Shuo Wang 《Food Science and Human Wellness》 SCIE CAS CSCD 2026年第5期2168-2183,共16页
2-Amino-3-methylimidazo[4,5-f]quinoline(IQ)is one of mutagenic/carcinogenic heterocyclic amines(HCAs)found mainly in well-cooked meats.As a common HCAs,IQ can pose a health risk to animals as well as humans.However,to... 2-Amino-3-methylimidazo[4,5-f]quinoline(IQ)is one of mutagenic/carcinogenic heterocyclic amines(HCAs)found mainly in well-cooked meats.As a common HCAs,IQ can pose a health risk to animals as well as humans.However,to date,few studies have explored IQ's toxic effects on systemic health,and its relevant mechanism of toxicity has not been elucidated.In this study,we for the first time determined IQ accumulation and investigated the tissue damage of developing zebrafish.Zebrafish at one-month post-fertilization were exposed to IQ(80 ng/mL)for 35 days.Ultra performance liquid chromatography-tandem mass spectrometry(UPLC-MS/MS)analysis showed that IQ accumulated in multi-organ of zebrafish such as eye,spleen,gonad(ovary or testis),heart,intestine,kidney,muscle,liver,and brain.Our results showed that IQ exposure caused histopathological alterations in IQ-accumulated organs,which could compromise organ function.Exposure to IQ significantly inhibited antioxidant related indicators.Moreover,IQ exposure significantly increased mTOR gene levels.The immunohistochemical results further validated that IQ exposure tended to over activate mTOR.In addition,IQ exposure significantly reduced the expression of autophagy-related genes,and upregulated the expression of DNA damage and repair-related genes,which also detected the accumulation of fluorescence signal of DNA damage markerγ-H2AX.Furthermore,TUNEL assay showed that IQ exposure caused apoptosis.Our findings revealed that IQ could be taken up by developing zebrafish,and accumulate in multiple tissues,especially across the blood-brain barrier,accumulate in the brain,subsequently causing systemic tissue damage,urging us to pay attention to the control or intervention of IQ exposure and decreasing accumulated impairment to systemic health. 展开更多
关键词 2-Amino-3-methylimidazo[4,5-f]quinoline Danio rerio Ultra performance liquid chromatography-tandem mass spectrometry Oxidative stress DNA damage Apoptosis mTOR activation
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AdipoRon Promotes Mitochondrial Ca2+Overload and Apoptosis in Hepatocellular Carcinoma Cells by Activating the PLC-IP3-IP3R Signaling Pathway 认领 引用
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作者 Zongmeng Zhang Cai Chen +3 位作者 ShaoruiRui ConghanLi Jiong Gu Liang He 《BIOCELL》 SCIE 2026年第1期193-211,共19页
Objective:Hepatocellular carcinoma(HCC)ranks among themost prevalentmalignant tumors globally.Metabolically associated fatty liver disease is a significant risk factor for HCC.Adiponectin,a key regulatory protein in g... Objective:Hepatocellular carcinoma(HCC)ranks among themost prevalentmalignant tumors globally.Metabolically associated fatty liver disease is a significant risk factor for HCC.Adiponectin,a key regulatory protein in glucolipid metabolism,presents potential as an anti-tumor target in HCC cells.The study focused on evaluating the anti-HCC properties of AdipoRon,an agonist of the adiponectin receptor.Method:Cell viability and proliferation were assessed using the cell counting kit-8 and colony formation assays,respectively.AdipoRon’s effect on HCC cell damage was evaluated via flow cytometry,apoptosis,and(lactate dehydrogenase)LDH assays.Mitochondrial function was evaluated by measuring mitochondrial membrane potential(MMP),ATP levels,and Complex I activity.Additionally,mitochondrial reactive oxygen species(ROS)and calcium(Ca2+)levelswere analyzed usingMitoSOXRed and Rhod-2 AM probes,respectively.Results:Our findings indicated that AdipoRon suppressed the proliferation of HCC cells and triggered apoptosis,with both effects being dose-dependent.Furthermore,AdipoRon caused a decrease in mitochondrial membrane potential,ATP levels,and Complex I activity,alongside the generation of mitochondrial ROS.Notably,AdipoRon disrupted intracellular Ca2+homeostasis by causing mitochondrial Ca2+overload due to release fromthe endoplasmic reticulum(ER).Additionally,AdipoRon promoted Ca2+release from the ER by activating the PLC-IP3-IP3R pathway.The resulting mitochondrial Ca2+overload enhances the anti-HCC effect when combined with chemotherapeutic drugs.Conclusions:Therefore,our study demonstrates thatAdipoRon promotesmitochondrial Ca2+overload and apoptosis in HCC cells by activating the PLC-IP3-IP3R signaling pathway.AdipoRon has the potential to become an effective anti-HCC drug. 展开更多
关键词 Hepatocellular carcinoma AdipoRon mitochondrial Ca2+overload apoptosis
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Beyond apoptosis: Implications of annexin-Ⅴ binding to myeloid cells in DARC(Detection of Apoptosing Retinal Cells) imaging 认领 引用
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作者 Kiyoharu J.Miyagishima Francisco M.Nadal-Nicolás Wei Li 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第6期2351-2352,共2页
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
关键词 neurodegenerative diseases vivo imaging annexin v window neural health neurodegenerative conditions apoptosis monitor disease progression myeloid cells
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