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World Journal of Gastroenterology 1998年第4期4卷 15-21页

作者： WANG LiDong1, ZHOU Qi1, WEI JunPing1, YANG WanCai1, ZHAO Xin1, WANG LiXia1, ZOU Jian Xiang1, GAO ShanShan1, LI YongXin1 and YANG C.S.2Keywords esophageal neoplasms apoptosis precancerous lesions Waf1 p21 gene p53

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Ａｐｏｐｔｏｓｉｓａｎｄｉｔｓｒｅｌａｔｉｏｎｓｈｉｐｗｉｔｈｃｅｌｐｒｏｌｉｆｅｒａｔｉｏｎ，ｐ５３，Ｗａｆ１ｐ２１，ｂｃｌ２ａｎｄｃｍｙｃｉｎｅｓｏｐｈａｇｅａｌｃａｒｃｉｎｏｇｅｎｅｓｉｓｓｔｕｄｉｅｄｗｉｔｈａｈｉｇｈｒｉｓｋｐｏｐｕｌ...

关键词： esophageal apoptosis carcinogenesis mycin

Asperuloside Promotes apoptosis of Cervical Cancer Cells through Endoplasmic Reticulum Stress-Mitochondrial Pathway

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Chinese Journal of Integrative Medicine 2024年第1期30卷 34-41页

作者： QI Zhi-min WANG Xia LIU Xia ZHAO Juan Medical Examination Center Hebei Province Hospital of Chinese MedicineShijiazhuang(050011)China Department of Gynaecology and Obstetrics Hebei Province Hospital of Chinese MedicineShijiazhuang(050011)China Experimental Center for Teaching Hebei Medical UniversityShijiazhuang(050017)China

Objective: To investigate the effects of asperuloside on cervical cancer based on endoplasmic reticulum(ER) stress and mitochondrial pathway. Methods: Different doses(12.5–800 μg/mL) of asperuloside were used to treat cervical cancer cell lines Hela and CaSki to calculate the half maximal inhibitory concentration(IC_(50)) of asperuloside. The cell proliferation was analyzed by clone formation assay. Cell apoptosis, intracellular reactive oxygen species(ROS) and mitochondrial membrane potential were determined by flow cytometry. The protein expressions of cleaved-caspase-3, Bcl-2, Bax, Cyt-c, cleaved-caspase-4 and glucose-regulated protein 78(GRP78) were analyzed by Western blot. And the inhibitor of ER stress, 4-phenyl butyric acid(4-PBA) was used to treat cervical cancer cells to further verify the role of ER stress in the apoptosis of cervical cancer cells induced by asperuloside. Results: Asperuloside of 325, 650, and 1300 μg/mL significantly inhibited the proliferation and promoted apoptosis of Hela and CaSki cells(Papoptosis(Papoptosis and cleaved-caspase-3,-4 and GRP78 protein expressions(Papoptosis of cervical cancer cells through ER stress-mitochondrial pathway.

关键词： asperuloside Chinese medicine cervical cancer endoplasmic reticulum stress mitochondrial damage apoptosis

B-cell lymphoma-2 phosphorylation at Ser70 site-related autophagy mediates puerarin-inhibited the apoptosis of MC3T3-E1 cells during osteoblastogenesis

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Journal of Traditional Chinese Medicine 2024年第1期44卷 27-34页

作者： LI Xi LIN Xiangquan CHEN Dongdong LIU Hui the Third Clinical Medical College Fujian Medical University Department of Orthopedics Fuzhou Second HospitalFuzhou 350007China

OBJECTIVE:To explore the relationship between autophagy and apoptosis regulated by puerarin during osteoblastogenesis.METHODS:In this study,the effects of puerarin on the autophagic activity and apoptosis level of osteoblast precursors(MC3T3-E1 cells)was observed.Subsequently,the roles of puerarin on B-cell lymphoma-2(Bcl-2)phosphorylation at different sites in osteoblast precursors were observed.The effect of puerarin on the interaction between Bcl-2 and autophagy regulatory molecule or pro-apoptotic molecule was also investigated using Co-immunoprecipitation assays.In addition,the effect of puerarin on mitochondrial membrane potential of osteoblast precursors was also identified by mitochondrial membrane potential fluorescence probe assays.RESULTS:Our results showed that puerarin can promote the autophagic activity and apoptosis level of MC3T3-E1cells.In addition,puerarin promoted Bcl-2phosphorylation at Ser70 site,and the dissociation of Bcl-2-Beclin1 complex.Moreover,puerarin could enhance the binding of Bcl-2-Bcl-2-Associated X(Bax)complex in MC3T3-E1 cells.Furthermore,puerarin increased the mitochondrial membrane potential of MC3T3-E1 cells.CONCLUSIONS:Therefore,puerarin promotes Beclin1into autophagy flux through Bcl-2 phosphorylation at Ser70,thereby enhancing autophagy of osteoblast precursors,which mediates its anti-apoptotic role during osteoblastogenesis.Furthermore,the dissociation of Bcl-2-Beclin1 complex is conducive to the binding of Bcl-2-Bax complex,which resists the apoptosis of osteoblast precursors via the increased mitochondrial membrane potential.

关键词： puerarin osteoblasts autophagy apoptosis lymphoma B-cell

Treatment with β-sitosterol ameliorates the effects of cerebral ischemia/reperfusion injury by suppressing cholesterol overload, endoplasmic reticulum stress, and apoptosis

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Neural Regeneration Research 2024年第3期19卷 642-649页

作者： Xiuling Tang Tao Yan Saiying Wang Qingqing Liu Qi Yang Yongqiang Zhang Yujiao Li Yumei Wu Shuibing Liu Yulong Ma Le Yang Precision Pharmacy&Drug Development Center Department of PharmacyTangdu HospitalAir Force Medical UniversityXi’anShaanxi ProvinceChina Department of Clinical Pharmacy Jinling HospitalMedical School of Nanjing UniversityNanjingJiangsu ProvinceChina Department of Pharmacology School of PharmacyAir Force Medical UniversityXi’anShaanxi ProvinceChina Department of Anesthesiology The First Medical Center of Chinese PLA General HospitalBeijingChina Department of Anatomy Histology and Embryology and K.K.Leung Brain Research CentreAir Force Medical UniversityXi’anShaanxi ProvinceChina

β-Sitosterol is a type of phytosterol that occurs naturally in plants.Previous studies have shown that it has anti-oxidant,anti-hyperlipidemic,anti-inflammatory,immunomodulatory,and anti-tumor effects,but it is unknown whetherβ-sitosterol treatment reduces the effects of ischemic stroke.Here we found that,in a mouse model of ischemic stroke induced by middle cerebral artery occlusion,β-sitosterol reduced the volume of cerebral infarction and brain edema,reduced neuronal apoptosis in brain tissue,and alleviated neurological dysfunction;moreover,β-sitosterol increased the activity of oxygen-and glucose-deprived cerebral cortex neurons and reduced apoptosis.Further investigation showed that the neuroprotective effects ofβ-sitosterol may be related to inhibition of endoplasmic reticulum stress caused by intracellular cholesterol accumulation after ischemic stroke.In addition,β-sitosterol showed high affinity for NPC1L1,a key transporter of cholesterol,and antagonized its activity.In conclusion,β-sitosterol may help treat ischemic stroke by inhibiting neuronal intracellular cholesterol overload/endoplasmic reticulum stress/apoptosis signaling pathways.

关键词： apoptosis blood-brain barrier β-sitosterol cerebral ischemia/reperfusion injury cholesterol overload cholesterol transport endoplasmic reticulum stress ischemic stroke molecular docking NPC1L1

The appearance of cytoplasmic cytochrome C precedes apoptosis during Drosophila salivary gland degradation

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Insect Science 2024年第1期31卷 157-172页

作者： Shihui Long Wenxin Cao Yongyu Qiu Ruohan Deng Jiali Liu Lidan Zhang Renke Dong Fengxin Liu Sheng Li Haigang Zhao Na Li Kang Li Guangdong Provincial Key Laboratory of Insect Developmental Biology and Applied Technology Institute of Insect Science and TechnologySchool of Life SciencesSouth China Normal UniversityGuangzhouChina Guangdong Laboratory for Lingnan Modern Agriculture South China Agricultural UniversityGuangzhouChina Guangmeiyuan R&D Center Guangdong Provincial Key Laboratory of Insect Developmental Biology and Applied TechnologySouth China Normal UniversityMeizhouGuangdong ProvinceChina School of Food Science and Engineering South China University of TechnologyGuangzhouChina ChemPartner PharmaTech Co. LtdJiangmenGuangdong ProvinceChina

apoptosis is an important process for organism development that functions to eliminate cell damage,maintain homeostasis,and remove obsolete tissues during morphogenesis.In mammals,apoptosis is accompanied by the release of cytochrome C(Cyt-c)from mitochondria to the cytoplasm.However,whether this process is conserved in the fruit fly,Drosophila melanogaster,remains controversial.In this study,we discovered that during the degradation of Drosophila salivary gland,the transcription of mitochondria apoptosis factors(MAPFs),Cyt-c,and death-associated APAF1-related killer(Dark)encoding genes are all upregulated antecedent to initiator and effector caspases encoding genes.The proteins Cyt-c and the active caspase 3 appear gradually in the cytoplasm during salivary gland degradation.Meanwhile,the Cyt-c protein colocates with mito-GFP,the marker indicating cytoplasmic mitochondria,and the change in mitochondrial membrane potential coincides with the appearance of Cyt-c in the cytoplasm.Moreover,impeding or promoting 20E-induced transcription factor E93 suppresses or enhances the staining of Cyt-c and the active caspase 3 in the cytoplasm of salivary gland,and accordingly decreases or increases the mitochondrial membrane potential,respectively.Our research provides evidence that cytoplasmic Cyt-c appears before apoptosis during Drosophila salivary gland degradation,shedding light on partial conserved mechanism in apoptosis between insects and mammals.

关键词： active caspase 3 apoptosis Cyt-c Drosophila salivary gland

Malvidin Mitigates Sepsis-induced Cardiac Injury by Modulating the TLR4-iNOS-COX-2 Inflammatory Pathway and the Bax/Bcl-2/Cyto-C Mitochondrial apoptosis Pathway in a p38 MAPK-dependent Manner

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Biomedical and Environmental Sciences 2024年第2期37卷 221-227页

作者： ZHANG Wei YUAN Si Long QIANG Jing Chao HUANG He LI Da SUN Ying ZHANG Hong Gang Department of Vascular Surgery The First People’s Hospital of LianyungangLianyungang 222005JiangsuChina Jiangsu Key Laboratory of Marine Pharmaceutical Compound Screening College of PharmacyJiangsu Ocean UniversityLianyungang 222005JiangsuChina Jinzhou Medical University postgraduate training base(Lianyungang First People’s Hospital) Lianyungang 222005JiangsuChina

In critical care medicine,sepsis is a dangerous systemic condition that is highly prevalent and is associated with high morbidity and mortality rates^([1]).The high mortality rate associated with sepsis is closely related to multi-organ dysfunction,with heart injury being particularly critical and considered the starting point of multi-organ injury^([2]).

关键词： mortality apoptosis TLR4

High expression circRALGPS2 in atretic follicle induces chicken granulosa cell apoptosis and autophagy via encoding a new protein

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Journal of Animal Science and Biotechnology 2024年第3期15卷 971-986页

作者： Haorong He Yuanhang Wei Yuqi Chen Xiyu Zhao Xiaoxu Shen Qing Zhu Huadong Yin Key Laboratory of Livestock and Poultry Multi‑Omics Ministry of Agriculture and Rural AffairsCollege of Animal Science and TechnologySichuan Agricultural UniversityChengduSichuan 611130China Farm Animal Genetic Resources Exploration and Innovation Key Laboratory of Sichuan Province Sichuan Agricultural UniversityChengduSichuan 611130China

Background The reproductive performance of chickens mainly depends on the development of follicles.Abnor-mal follicle development can lead to decreased reproductive performance and even ovarian disease among chick-ens.Chicken is the only non-human animal with a high incidence of spontaneous ovarian cancer.In recent years,the involvement of circRNAs in follicle development and atresia regulation has been confirmed.Results In the present study,we used healthy and atretic chicken follicles for circRNA RNC-seq.The results showed differential expression of circRALGPS2.It was then confirmed that circRALGPS2 can translate into a protein,named cir-cRALGPS2-212aa,which has IRES activity.Next,we found that circRALGPS2-212aa promotes apoptosis and autophagy in chicken granulosa cells by forming a complex with PARP1 and HMGB1.Conclusions Our results revealed that circRALGPS2 can regulate chicken granulosa cell apoptosis and autophagy through the circRALGPS2-212aa/PARP1/HMGB1 axis.

关键词： apoptosis Autophagy Chicken CircRALGPS2 Follicle atresia PARP1 RNC-seq

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Shuxuening Injection Inhibits apoptosis and Reduces Myocardial Ischemia-Reperfusion Injury in Rats through PI3K/AKT Pathway

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Chinese Journal of Integrative Medicine 2024年第5期30卷 421-432页

作者： YUE Tong-tong CAO Ying-jie CAO Ya-xuan LI Wei-xia WANG Xiao-yan SI Chun-ying XIA Han ZHU Ming-jun TANG Jin-fa WANG He The First Clinical Medical College of Henan University of Chinese Medicine Zhengzhou 450046China Department of Pharmacy the First Affiliated Hospital of Henan University of Chinese MedicineZhengzhou 451200China Department of Cardiovascular Diseases the First Affiliated Hospital of Henan University of Chinese MedicineZhengzhou 451200China

Objective: To investigate the main components and potential mechanism of Shuxuening Injection(SXNI) in the treatment of myocardial ischemia-reperfusion injury(MIRI) through network pharmacology and in vivo research. Methods: The Traditional Chinese Medicine Systems Pharmacology(TCMSP) and Pharm Mapper databases were used to extract and evaluate the effective components of Ginkgo biloba leaves, the main component of SXNI. The Online Mendelian Inheritance in Man(OMIM) and Gene Cards databases were searched for disease targets and obtain the drug target and disease target intersections. The active ingredient-target network was built using Cytoscape 3.9.1 software. The STRING database, Metascape online platform, and R language were used to obtain the key targets and signaling pathways of the anti-MIRI effects of SXNI. In order to verify the therapeutic effect of different concentrations of SXNI on MIRI in rats, 60 rats were first divided into 5 groups according to random number table method: the sham operation group, the model group, SXNI low-dose(3.68 mg/kg), medium-dose(7.35 mg/kg), and high-dose(14.7 mg/kg) groups, with 12 rats in each group. Then, another 60 rats were randomly divided into 5 groups: the sham operation group, the model group, SXNI group(14.7 mg/kg), SXNI+LY294002 group,and LY294002 group, with 12 rats in each group. The drug was then administered intraperitoneally at body weight for 14 days. The main biological processes were validated using in vivo testing. Evans blue/triphenyltetrazolium chloride(TTC) double staining, hematoxylin-eosin(HE) staining, terminal deoxynucleotidyl transferase d UTP nick end labeling(TUNEL) assay, enzyme-linked immunosorbent assay(ELISA), and Western blot analysis were used to investigate the efficacy and mechanism of SXNI in MIRI rats. Results: Eleven core targets and 30 Kyoto Encyclopedia of Genes and Genomes(KEGG) pathways were selected. Among these, the phosphoinositide 3-kinase(PI3K)/protein kinase B(AKT) pathway was closely related to SXNI treatment of MIRI. In v

关键词： myocardial ischemia reperfusion injury PI3K/AKT signaling pathway Shuxuening Injection apoptosis Ginkgo biloba leaves

TuBG1 promotes hepatocellular carcinoma via ATR/P53-apoptosis and cycling pathways

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Hepatobiliary & Pancreatic Diseases International 2024年第2期23卷 195-209页

作者： Yan Zhang Zhen-Zhen Wang An-Qi Han Ming-Ya Yang Li-Xin Zhu Fa-Ming Pan Yong Wang Department of General Surgery The Second Hospital of Anhui Medical UniversityHefei 230601China Department of General Surgery The First Affiliated Hospital of Anhui Medical UniversityHefei 230022China Department of Epidemiology and Biostatistics School of Public HealthAnhui Medical UniversityHefei 230032China The Key Laboratory of Major Autoimmune Diseases Anhui Medical UniversityHefei 230032China

Background:As reported,γ-tubulin(TuBG1)is related to the occurrence and development of various types of malignant tumors.However,its role in hepatocellular cancer(HCC)is not clear.The present study was to investigate the relationship between TuBG1 and clinical parameters and survival in HCC patients.Methods:The correlation between TuBG1 and clinical parameters and survival in HCC patients was ex-plored by bioinformatics analysis.Immunohistochemistry was used for the verification.The molecular function of TuBG1 was measured using colony formation,scratch assay,trans-well assay and flow cytometry.Gene set enrichment analysis(GSEA)was used to pick up the enriched pathways,followed by investigating the target pathways using Western blotting.The tumor-immune system interactions and drug bank database(TISIDB)was used to evaluate TuBG1 and immunity.Based on the TuBG1-related immune genes,a prognostic model was constructed and was further validated internally and externally.Results:The bioinformatic analysis found high expressed TuBG1 in HCC tissue,which was confirmed us-ing immunohistochemistry and Western blotting.After silencing the TuBG1 in HCC cell lines,more G1 arrested cells were found,cell proliferation and invasion were inhibited,and apoptosis was promoted.Furthermore,the silence of TuBG1 increased the expressions of Ataxia-Telangiectasia and Rad-3(ATR),phospho-P38 mitogen-activated protein kinase(P-P38MAPK),phospho-P53(P-P53),B-cell lymphoma-2 associated X protein(Bax),cleaved caspase 3 and P21;decreased the expressions of B-cell lymphoma-2(Bcl-2),cyclin D1,cyclin E2,cyclin-dependent kinase 2(CDK2)and CDK4.The correlation analysis of immunohistochemistry and clinical parameters and survival data revealed that TuBG1 was negatively corre-lated with the overall survival.The constructed immune prognosis model could effectively evaluate the prognosis.Conclusions:The increased expression of TuBG1 in HCC is associated with poor prognosis,which might be involved in the occurrence and development of HCC.

关键词： TuBG1 Hepatocellular carcinoma apoptosis Cell cycling Immunomodulators

Hernandezine promotes cancer cell apoptosis and disrupts the lysosomal acidic environment and cathepsin D maturation

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Chinese Journal of Natural Medicines 2024年第5期22卷 387-401页

作者： FENG Qianwen SUN Lu Muhammad Jibran Sualeh ZHAO Qingli ZHAO Songji CUI Zhengguo INADERA Hidekuni Department of Public Health Graduate School of Medicine and Pharmaceutical SciencesUniversity of ToyamaToyama 930-8501Japan Department of Pediatric Cardiology Heart CenterGuangzhou Women and Children’s Medical CenterGuangzhou Medical UniversityGuangzhou 510000China Department of Basic Medical Sciences College of MedicineUniversity of SharjahSharjah 57545United Arab Emirates Department of Radiology Graduate School of Medicine and Pharmaceutical SciencesUniversity of ToyamaToyama 930-8501Japan Advanced Clinical Research Center Fukushima Global Medical Science CenterFukushima Medical UniversityFukushima CityFukushima 960-8074Japan Department of Environmental Health School of Medical SciencesUniversity of FukuiFukui 910-8580Japan

Hernandezine(Her),a bisbenzylisoquinoline alkaloid extracted from Thalictrum flavum,is recognized for its range of biological activities inherent to this herbal medicine.Despite its notable properties,the anti-cancer effects of Her have remained largely unexplored.In this study,we elucidated that Her significantly induced cytotoxicity in cancer cells through the activation of apoptosis and necroptosis mechanisms.Furthermore,Her triggered autophagosome formation by activating the AMPK and ATG5 conjugation systems,leading to LC3 lipidation.Our findings revealed that Her caused damage to the mitochondrial membrane,with the damaged mitochondria undergoing mitophagy,as evidenced by the elevated expression of mitophagy markers.Conversely,Her disrupted autophagic flux,demonstrated by the upregulation of p62 and accumulation of autolysosomes,as observed in the RFP-GFP-LC3 reporter assay.Initially,we determined that Her did not prevent the fusion of autophagosomes and lysosomes.However,it inhibited the maturation of cathepsin D and increased lysosomal pH,indicating an impairment of lysosomal function.The use of the early-stage autophagy inhibitor,3-methyladenine(3-MA),did not suppress LC3II,suggesting that Her also induces noncanonical autophagy in autophagosome formation.The application of Bafilomycin A1,an inhibitor of noncanonical autophagy,diminished the recruitment of ATG16L1 and the accumulation of LC3II by Her,thereby augmenting Her-induced cell death.These observations imply that while autophagy initially plays a protective role,the disruption of the autophagic process by Her promotes programmed cell death.This study provides the first evidence of Her’s dual role in inducing apoptosis and necroptosis while also initiating and subsequently impairing autophagy to promote apoptotic cell death.These insights contribute to a deeper understanding of the mechanisms underlying programmed cell death,offering potential avenues for enhancing cancer prevention and therapeutic strategies.

关键词： Hernandezine apoptosis Mitophagy Autophagic flux Lysosome Noncanonical autophagy