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| 1 | Function of apoptosis and expression of the proteins Bcl-2,p53 and C-myc in the development of gastric cancer显示文摘INTRODUCTIONIn China ,the incidence and mortality of gastric cancer rank the second among all cancers. Recent development of cancer [1-20].The aim of this study was investigat the insight of apoptosis and bcl-2, p53 and C-myc protein expression in the development of gastric cancer . | An Gao Xu Shao Guang Li Ji Hong Liu Ai Hua Gan Research Laboratory of Digestive Disease,Huizhou Central People’s Hospital,Huizhou 516001,Guangdong Province,ChinaDr.An Gao Xu graduated from Guangdong Medical College in 1984.He is an associate physician-in-chief,specializing in the research and treatment of gastrointestinal and liver tumors.He has published 24 papers and 1 book. | 2001 | World Journal of Gastroenterology2001，7，3： | 91 |
| 2 | Apoptosis and its relationship with cell proliferation,p53,Waf1p21,bcl-2 and c-mycin esophageal carcinogenesis studied with a high-risk population in northern China显示文摘Apoptosisanditsrelationshipwithcelproliferation,p53,Waf1p21,bcl2andcmycinesophagealcarcinogenesisstudiedwithahighriskpopul... | WANG LiDong1, ZHOU Qi1, WEI JunPing1, YANG WanCai1, ZHAO Xin1, WANG LiXia1, ZOU Jian Xiang1, GAO ShanShan1, LI YongXin1 and YANG C.S.2Keywords esophageal neoplasms apoptosis precancerous lesions Waf1 p21 gene p53 | 1998 | World Journal of Gastroenterology1998，4，4： | 295 |
| 3 | Necroptosis, pyroptosis and apoptosis: an intricate game of cell death显示文摘Cell death is a fundamental physiological process in all living organisms.Its roles extend from embryonic development,organ maintenance,and aging to the coordination of immune responses and autoimmunity.In recent years,our understanding of the mechanisms orchestrating cellular death and its consequences on immunity and homeostasis has increased substantially.Different modalities of what has become known as‘programmed cell death’have been described,and some key players in these processes have been identified.We have learned more about the intricacies that fine tune the activity of common players and ultimately shape the different types of cell death.These studies have highlighted the complex mechanisms tipping the balance between different cell fates.Here,we summarize the latest discoveries in the three most well understood modalities of cell death,namely,apoptosis,necroptosis,and pyroptosis,highlighting common and unique pathways and their effect on the surrounding cells and the organism as a whole. | Damien Bertheloot Eicke Latz Bernardo S.Franklin | 2021 | Cellular & Molecular Immunology2021，18，5： | 84 |
| 4 | NLRP3 inflammasome activation and cell death显示文摘The NLRP3 inflammasome is a cytosolic multiprotein complex composed of the innate immune receptor protein NLRP3,adapter protein ASC,and inflammatory protease caspase-1 that responds to microbial infection,endogenous danger signals,and environmental stimuli.The assembled NLRP3 inflammasome can activate the protease caspase‐1 to induce gasdermin D-dependent pyroptosis and facilitate the release of IL-1β and IL-18,which contribute to innate immune defense and homeostatic maintenance.However,aberrant activation of the NLRP3 inflammasome is associated with the pathogenesis of various inflammatory diseases,such as diabetes,cancer,and Alzheimer’s disease.Recent studies have revealed that NLRP3 inflammasome activation contributes to not only pyroptosis but also other types of cell death,including apoptosis,necroptosis,and ferroptosis.In addition,various effectors of cell death have been reported to regulate NLRP3 inflammasome activation,suggesting that cell death is closely related to NLRP3 inflammasome activation.In this review,we summarize the inextricable link between NLRP3 inflammasome activation and cell death and discuss potential therapeutics that target cell death effectors in NLRP3 inflammasome-associated diseases. | Yi Huang Wen Xu Rongbin Zhou | 2021 | Cellular & Molecular Immunology2021，18，9： | 94 |
| 5 | Growth inhibition and apoptosis induction Sulindac on Human gastric cancer cells显示文摘AIM: To evaluate the effects of sulindac in inducing growth inhibition and apoptosis of human gastric cancer cells in comparison with human hepatocellular carcinoma (HCC)cells.METHODS: The human gastric cancer cell lines MKN45 and MKN28 and human hepatocellular carcinoma cell lines HepG2and SMMC7721 were used for the study. Anti-proliferative effect was measured by MTT assay, and apoptosis was determined by Hoechst-33258 staining, electronography and DNA fragmentation. The protein of cyclooxygenase-2 (COX(2) and Bcl-2 were detected by Westem dot blotting.RESULTS: Sulindac could initiate growth inhibition and apoptosis of MKN45, MKN28, HepG2 and SMMC7721 cells in a dose-and time-dependent manner. Growth inhibitory activity and apoptosis were more sensitive in HepG2 cells than in SMMC7721 cells, MKN45 and MKN28 cells. After 24hours incubation with sulindac at 2mmol. L-1 and 4mmol.L-1, the level of COX-2 and Bcl-2 protein were lowered in MKN45, SMMC7721 and HepG2 cells but not in MKN28 cells.CONCLUSION: Sulindac could inhibit the growth of gastric cancer cells and HCC cells effectively in vitro by apoptosis induction, which was associated with regression of COX-2and Bcl-2 expression. The growth inhibition and apoptosis of HCC cells were greater then that of human gastric cancer cells. The different effects of apoptosis in gastric cancer cells may be related to the differentiation of the cells. | Yun-Lin Wu~1 Bo Sun~1 Xue-Jun Zhang~2 Sheng-Nian Wang~2 Heng-Yi He~2 Min-Min Qiao~1 Jie Zhong~1 Jia-Yu Xu~1 1 Department of Gastroenterology,Ruijin Hospital,Shanghai Second Medical University,Shanghai 200025,China2 Institude of Biochemistry and Cell Biology,Shanghai Institues for Biological Sciences,Chinese Academy of Sciences.Shanghai 200025,China | 2001 | World Journal of Gastroenterology2001，7，6： | 64 |
| 6 | Antitumor effect of matrine in human hepatoma G2 cells by inducing apoptosis and autophagy显示文摘AIM: To study the antitumor effect of matrine in human hepatoma G2 (HepG2) cells and its molecular mechanism involved in antineoplastic activities. METHODS: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to detect viability of HepG2 cells. The effect of matrine on cell cycle was detected by flow cytometry. Annexin-V-FITC/PI double staining assay was used to detect cellular apoptosis. Cellular morphological changes were observed under an inverted phase contrast microscope. Transmission electron microscopy was performed to further examine ultrastructural structure of the cells treatedwith matrine. Monodansylcadaverine (MDC) staining was used to detect autophagy. Whether autophagy is blocked by 3-methyladenine (3-MA), an autophagy inhibitor, was evaluated. Expression levels of Bax and Beclin 1 in HepG2 cells were measured by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR).RESULTS: Matrine signif icantly inhibited the proliferation of HepG2 cells in a dose- and time-dependent manner, and induced G1-phase cell cycle arrest and apoptosis of HepG2 cells in a dose-dependent manner. The total apoptosis rate was 0.14% for HepG2 cells not treated with matrine. In contrast, the apoptosis rate was 28.91%, 34.36% and 38.80%, respectively, for HepG2 cells treated with matrine at the concentration of 0.5, 1.0 and 2.0 mg/mL. The remarkable morphological changes were observed under an inverted phase contrast microscope. Abundant cytoplasmic vacuoles with varying sizes were observed in HepG2 cells treated with matrine. Furthermore, vacuolization in cytoplasm progressively became larger and denser when the concentration of matrine was increased. Electron microscopy demonstrated formation of abundant autophagic vacuoles in HepG2 cells after matrine treatment. When the specif ic autophagic inhibitor, 3-MA, was applied, the number of autophagic vacuoles greatly decreased. MDC staining showed that the fluorescent density was higher and the number of MDC-labeled particles in HepG2 cells was greater in matrine treatment group than in control group. Fewer autophagic vacuoles were observed in the combined 3-MA and matrine treatment group when 3-MA was added before matrine treatment, indicating that both autophagy and apoptosis are activated when matrine-induced death of hepatoma G2 cells occurs. Real-time quantitative RT-PCR revealed that the expression levels of Bax gene, an apoptosis-related molecule, and Beclin 1 gene which plays a key role in autophagy were higher in matrine treatment group than in control group, indicating that Beclin 1 is involved in matrineinduced autophagy and the pro-apoptotic mechanismof matrine may be related to its upregulation of Bax expression. CONCLUSION: Matrine has potent antitumor activities in HepG2 cells and may be used as a novel effective reagent in treatment of hepatocellular carcinoma. | Zhang, Jun-Qiang Li, Yu-Min Liu, Tao He, Wen-Ting Chen, Ying-Tai Chen, Xiao-Hui Li, Xun Zhou, Wen-Ce Yi, Jian-Feng Ren, Zhi-Jian | 2010 | World Journal of Gastroenterology2010，16，34： | 61 |
| 7 | Analysis of in vivo patterns of caspase 3 gene expression in primary hepatocellular carcinoma and its relationship to p21^(WAF1) expression and hepatic apoptosis显示文摘AIM To detect the expression of caspase 3gene in primary human hepatocellular carcinoma(HCC)and investigate its relationship to p21WAF1gene expression and HCC apoptosis.METHODS In situ hybridization was employedto determine caspase 3 and p21WAF1expression inHCC.In situ end-labeling was used to detecthepatocytic apoptosis in HCC.RESULTS Twenty-one of 39(53.8%)cases ofHCC were found to express caspase 3transcripts,while 45.2% of HCC failed toexpress caspase 3.Non-cancerous adjacent livertissues showed more positive caspase 3(87.5%,7/8)as compared with HCC(P<0.05).The expression of caspase 3 is correlated withHCC differentiation,72.2%(13/18)ofmoderately to highly differentiated HCC showedcaspase 3 transcripts positive,while only 38.1%of poorly differentiated HCC harbored caspase 3transcripts(P<0.05).No relationship wasfound between caspase 3 expression and tumorsize or grade or metastasis,although 52.5%(5/8)of HCC with metastasis were caspase 3positive and a little higher than that with nometastasis(51.6%,P>0.05).Expression of caspase 3 alone did not affect the apoptosisindex(AI)of HCC.The AI was 7.12%o in caspase3-positive tumors(n=21),while in caspase 3-negative cases(n=18)6.59%0(P>0.05).Expression of caspase 3 clearly segregated withp21WAF1positive tumors as compared withp21WAF1-negative cases(16 of 23,69.6% versus5 of 16,31.3%)with statistical significance(P=0.017).In the cases with positive caspase 3and negative p21WAF1,the Al was found slightlyhigher,but with no statistical significance,thanthat with expression of p21WAF1and caspase 3(7.21‰ vs 6.98‰,P>0.05).CONCLUSION Loss of caspase 3 expressionmay contribute to HCC carcinogenesis,althoughthe expression of caspase 3 does not correlatewell with cell apoptosis in HCC.p21WAF1may bemerely one of the inhibitors which can reducecaspase 3 mediated cell apoptosis in HCCs. | Bao Hua Sun Jun Zhang Bao JǜWang Xi Ping Zhao You Kun Wang Zhi Qun Yu Dong Liang Yang Lian Jie Hao Department of Clinical Immunology,Tongji Hospital,Tongji Medical University,Wuhan 430030,Hubei Province,China | 2000 | World Journal of Gastroenterology2000，6，3： | 65 |
| 8 | Apoptosis,proliferation and p53 gene expression of H.pylori associated gastric epithelial lesions显示文摘AIM: To study the relationship between Helicobacter pylori (H. Pylori) and gastric carcinoma and its possible pathogenesis by H. Pylori.METHODS: DNEL technique and immunohistochemical technique were used to study the state of apoptosis,proliferation and p53 gene expression. A total of 100 gastric mucosal biopsy specimens, including 20 normal mucosa, 30H. Pylori-negative and 30 H. Pylorf-positive gastric precancerous lesions along with 20 gastric carcinomas were studied.RESULTS: There were several apoptotic cells in the superficial epithelium and a few proliferative cells within the neck of gastric glands, and no p53 protein expression in normal mucosa. In gastric carcinoma, there were few apoptotic cells, while there were a large number of proliferative cells, and expression of p53 protein significantly was increased. In the phase of metaplasia, the apoptotic index (Al, 4.36% ± 1.95%), proliferative index (PI, 19.11% ± 6.79%) and positivity of p53 expression (46.7%) in H. Pylori-positive group were higher than those in normal mucosa (P< 0.01). Al in H. Pylori-positive group was higher than that in H. Pylori-negative group (3.81% ±1.76%), PI in H. Pylori-positive group was higher than that in H. Pylori-negative group (12.25% ±5.63%, P<0.01 ). In the phase of dysplasia, Al (2.31% ± 1.10%) in H. Pylori-positive group was lower (3.05% ± 1.29%) than that in H. Pylori-negative group, but PI (33.89% ± 11.65%)wassignificantly higher(22.09± 8018%, P< 0.01). In phases of metaplasia, dysplasia and gastric cancer in the H. Pylori-positive group, Als had an evidently graduall decreasing trend (P < 0.01 ), while Pis had an evidently gradual increasing trend (P< 0.05 or P< 0.01), and there was also a trend of gradual increase in the expression of p53 gene.CONCLUSION: In the course of the formation of gastric carcinoma, proliferation of gastric mucosa can be greatly increased by H. Pylori, and H. Pylori can induce apoptosis in the phase of metaplasia but in the phase of dysplasia H.pylori can inhibit cellular apoptosis. And H. Pylori infection can strengthen the expression of mutated p53 gene. | Zhong Zhang~1 Yuan Yuan Hua Gao Ming Dong Lan Wang Yue-Hua Gong 1 Department of Pathology,Shenyang Medical College,Shenyang 110031 Liaoning Province,China | 2001 | World Journal of Gastroenterology2001，7，6： | 46 |
| 9 | Induction of apoptosis by arsenic trioxide and hydroxycamptothecin in gastric cancer cells in vitro显示文摘AIM To study the effects of arsenic trioxide andHCPT on different degrees of differentiated gastriccancer cells(SGC-7901,MKN-45,MKN-28)withrespect to both cytotoxicity and induction ofapoptosis in vitro.METHODS The cytotoxicity of As2O3 and HCPTon gastric cancer cells was determined by MTTassay.Morphologic changes of apoptosis ofgastric cancer cells were observed by lightmicroscopy and transmission electron microscopy.Apoptosis and cell cycle changes of gastric cancercells induced by HCPT and As2O3 were investigatedby TUNEL method and flow cytometry.RESULTS As2O3 and HCPT had remarkablecytotoxic effects on different degrees ofdifferentiated gastric cancer cells.The IC50ofAs2O3 on well differentiated gastric cancer cellMKN-28,moderately differentiated gastric cancercell SGC-7901,and poorly differentiated gastriccancer cell MKN-28 were 8.91 μmol/L,10.57μmol/L,and 11.65 μmol/L,respectively.The IC50of HCPT on MKN-28,SGC-7901,and MKN-45 were9.35 mg/L,10.21 mg/L,and 12.63 mg/Lrespectively after 48 h treatment.After 12 h ofexposure to both drugs,gastric cancer cellsexhibited morphologic features of apoptosis,including cell shrinkage,nuclear condensation, and formation of apoptotic bodies.A typicalsubdiploid peak before G0/G1 phase was observedby flow cytometry.The apoptotic rates of SGC-7901,MKN-45,and MKN-28 were 13.84%,22.52%,and 9.68%,respectively after 48 hexposure to 10 μmol/L As2O3.The apoptotic ratesof SGC-7901,MKN-45,and MKN-28 were 21.88%,12.35%,and 30.26%,respectively after 48 hexposure to 10 mg/L HCPT.The apoptotic indicewere 7%-15% as assessed by TUNEL method.The effect of As2O3 on SGC-7901 showedremarkable cell cycle specificity,which inducedcell death in G1 phase,and blocked G2/M phase.HCPT also showed a remarkable cell cyclespecificity,by inducing cell death and apoptosis inG1 phase and arrest of proliferation at S phase.CONCLUSION As2O3 and HCPT exhibitsignificant cytotoxicity on gastric cancer cells byinduction of apoptosis.As2O3 and HCPT mighthave a promising prospect in the treatment ofgastric cancer,which needs to be further studied. | Tu SP Zhong J Tan JH Jiang XH Qiao MM Wu YX Jiang SH | 2000 | World Journal of Gastroenterology2000，6，4： | 43 |
| 10 | Glycyrrhizic acid inhibits apoptosis and fibrosis in carbontetrachloride-induced rat liver injury显示文摘AIM:To investigate anti-apoptotic effects of glycyrrhizic acid(GA) against fibrosis in carbon tetrachloride(CCl4)-induced liver injury and its contributing factors.METHODS:Liver fibrosis was induced by administration of CCl4 for 8 wk.Pathological changes in the liver of rats were examined by hematoxylin-eosin staining.Collagen fibers were detected by Sirius red staining.Hepatocyte apoptosis was determined by TUNEL assay and the expression levels of cleaved caspase-3,Bax,α-SMA,connective tissue growth factor(CTGF),matrix metalloproteinase(MMP) 2 and MMP9 proteins were evaluated by western blot analysis,and α-SMA m RNA,collagen type Ⅰ and Ⅲ m RNA were estimated by real-time PCR.RESULTS:Treatment with GA significantly improved the pathological changes in the liver and markedly decreased the positive area of Sirius red compared with rats in the CCl4-treated group.TUNEL assay showed that GA significantly reduced the number of TUNEL-positive cells compared with the CCl4-treated group.The expression levels of cleaved caspase-3,Bax,α-SMA,CTGF,MMP2 and MMP9 proteins,and α-SMA m RNA,collagen type Ⅰ and Ⅲ m RNA were also significantly reduced by GA compared with the CCl4-treated group(P < 0.05).CONCLUSION:GA treatment can ameliorate CCl4-induced liver fibrosis by inhibiting hepatocyte apoptosis and hepatic stellate cell activation. | Bo Liang Xiao-Ling Guo Jing Jin Yong-Chun Ma Zheng-Quan Feng | 2015 | World Journal of Gastroenterology2015，21，17： | 44 |
| 11 | Arsenic trioxide induces multiple myeloma cell apoptosis via disruption of mitochondrial transmembrane potentials and activation of caspase-3显示文摘investigate the response of multiple myeloma (MM) cells to arsenic trioxide (As 2O 3) and their possible mechanisms Methods Two MM derived cell lines RPMI8226 and U266 cells were used as in vitro models Cell apoptosis was assessed by morphology, flow cytometry, and DNA gel electrophoresis Mitochondrial transmembrane potentials (△Ψm) were evaluated by measuring cellular Rhodamine 123 staining intensity Protein expression was analyzed using Western blot Results Zero point one to 0 5?μmol/L As 2O 3 inhibited cell proliferation and 2.0?μmol/L As 2O 3 induced cell apoptosis, while 1.0?μmol/L As 2O 3 inhibited proliferation with a weak degree of apoptosis induction in RPMI8226 and U266 cell lines As 2O 3 induced apoptosis was accompanied by mitochondrial transmembrane potentials (△Ψm) collapse and caspase 3 activation in the presence of intact membrane Glutathione depleter buthionine sulfoximine enhanced, while disulfide bond reducing agent dithiothreitol partially antagonized As 2O 3 induced △Ψm collapse and apoptosis in MM cells All trans retinoic acid (ATRA) could also induce apoptosis in RPMI8226 cells, but it did not show any cooperative effects with As 2O 3 Conclusion As 2O 3 exerts apoptosis inducing and growth inhibiting effects on MM cells, and mitochondrium is a pivotal and common target of As 2O 3 for apoptosis | 贾培敏 陈国强 黄晓君 蔡循 杨洁 王龙 周宇红 沈玉雷 周励 余韵 陈赛娟 张学光 王振义 | 2001 | Chinese Medical Journal2001，，1： | 36 |
| 12 | TGF-β signaling in cancer metastasis显示文摘转变生长因素(TGF )- 发信号的事件是众所周知的控制多样的进程和众多的回答例如房间增长,区别, apoptosis,和移植。在癌症的 TGF- 发信号戏上下文依赖者角色:在 pre 恶意的房间, TGF- 首先作为肿瘤 suppressor 工作,当在癌症的以后的阶段发信号的 TGF- 支持侵略和转移时。最近的研究也建议了在 TGF- 发信号和另外的发信号的小径之间的串音例如河马, Wnt, EGFR/RAS,和 PI3K/AKT 小径,可以实质地贡献我们 TGF- 发信号和癌症的当前的理解。由于 TGF- 的广阔效果, TGF- 和它的下游的发信号部件的封锁提供多重治疗学的机会。因此,为为众多的疾病表明治疗的 anti-TGF- 的眼界显得明亮并且将提供珍贵信息并且想在这药上分子的设计。在这评论,我们集中于最近的卓见进在可以贡献新奇指向癌症的治疗的发展的癌症转移发信号的 TGF- 的规定。 | Feng Xie Li Ling Hans van Dam Fangfang Zhou Long Zhang | 2018 | Acta Biochimica et Biophysica Sinica2018，50，1： | 36 |
| 13 | Acupuncture and neuroregeneration in ischemic stroke显示文摘Acupuncture is potentially beneficial for post-stroke rehabilitation and is considered a promising preventive strategy for stroke.Electroacupuncture pretreatment or treatment after ischemic stroke by using appropriate electroacupuncture parameters generates neuroprotective and neuroregenerative effects that increase cerebral blood flow,regulate oxidative stress,attenuate glutamate excitotoxicity,maintain bloodbrain barrier integrity,inhibit apoptosis,increase growth factor production,and induce cerebral ischemic tolerance. | Qwang-Yuen Chang Yi-Wen Lin Ching-Liang Hsieh | 2018 | Neural Regeneration Research2018，13，4： | 38 |
| 14 | Apelin-13 inhibits apoptosis and excessive autophagy in cerebral ischemia/reperfusion injury显示文摘Apelin-13 is a novel endogenous ligand for an angiotensin-like orphan G-protein coupled receptor,and it may be neuroprotective against cerebral ischemia injury.However,the precise mechanisms of the effects of apelin-13 remain to be elucidated.To investigate the effects of apelin-13 on apoptosis and autophagy in models of cerebral ischemia/reperfusion injury,a rat model was established by middle cerebral artery occlusion.Apelin-13(50μg/kg)was injected into the right ventricle as a treatment.In addition,an SH-SY5Y cell model was established by oxygen-glucose deprivation/reperfusion,with cells first cultured in sugar-free medium with 95%N2 and 5%CO2 for 4 hours and then cultured in a normal environment with sugar-containing medium for 5 hours.This SH-SY5Y cell model was treated with 10-7 M apelin-13 for 5 hours.Results showed that apelin-13 protected against cerebral ischemia/reperfusion injury.Apelin-13 treatment alleviated neuronal apoptosis by increasing the ratio of Bcl-2/Bax and significantly decreasing cleaved caspase-3 expression.In addition,apelin-13 significantly inhibited excessive autophagy by regulating the expression of LC3B,p62,and Beclin1.Furthermore,the expression of Bcl-2 and the phosphatidylinositol-3-kinase(PI3K)/Akt/mammalian target of rapamycin(mTOR)pathway was markedly increased.Both LY294002(20μM)and rapamycin(500 nM),which are inhibitors of the PI3K/Akt/mTOR pathway,significantly attenuated the inhibition of autophagy and apoptosis caused by apelin-13.In conclusion,the findings of the present study suggest that Bcl-2 upregulation and mTOR signaling pathway activation lead to the inhibition of apoptosis and excessive autophagy.These effects are involved in apelin-13-induced neuroprotection against cerebral ischemia/reperfusion injury,both in vivo and in vitro.The study was approved by the Animal Ethical and Welfare Committee of Jining Medical University,China(approval No.2018-JS-001)in February 2018. | Zi-Qi Shao Shan-Shan Dou Jun-Ge Zhu Hui-Qing Wang Chun-Mei Wang Bao-Hua Cheng Bo Bai | 2021 | Neural Regeneration Research2021，16，6： | 35 |
| 15 | Galangin induces apoptosis of hepatocellular carcinoma cells via the mitochondrial pathway显示文摘AIM:To investigate the mechanism by which galangin,a polyphenolic compound derived from medicinal herbs,induces apoptosis of hepatocellular carcinoma(HCC) cells.METHODS:The 3-(4,5-Dimethyl-thiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay was used to measure cell viability.Apoptosis was evaluated by in situ uptake of propidium iodide and Hoechst 33258 and was then detected by fluorescence microscopy.Protein expressions were detected by Western blotting.To confirm the apoptotic pathway mediated by galangin,cells were transfected by bcl-2 gene to overexpress Bcl-2 or siRNA to down-regulate Bcl-2 expression.RESULTS:Galangin(46.25-370.0 μmol/L) exerted an anti-proliferative effect,induced apoptosis,and decreased mitochondrial membrane potential in a dose and time-dependent manner.Treatment with galangin induced apoptosis by translocating the pro-apoptotic protein Bax to the mitochondria,which released apoptosis-inducing factor and cytochrome c into the cytosol.Overexpression of Bcl-2 attenuated galangin-induced HepG2 cell apoptosis,while decreasing Bcl-2 expression enhanced galangin-induced cell apoptosis.CONCLUSION:Our data suggests that galangin mediates apoptosis through a mitochondrial pathway,and may be a potential chemotherapeutic drug for the treatment of HCC. | Hai-Tao Zhang Liu-Bo Lan Da-Hua Fan Kai-Dan Zhu Xiao-Yi Chen Min Wen Hui-Ming Liu Guangdong Province China Hui Luo | 2010 | World Journal of Gastroenterology2010，16，27： | 32 |
| 16 | Apoptosis induced by norcantharidin in human tumor cells显示文摘INTRODUCTIONThe antitumor activity of norcantharidin (NCTD),the demethylated analogue of cantharidin,wasstudied in the early 1980s in China.NCTD has noside effects on urinary organs which cantharidin hasshown and is easier to synthesize,and it can inhibitthe proliferation of several tumor cell lines as wellas transplanted tumors.Clinical trials with NCTD asa monotherapeutic agent indicated that NCTD hadbeneficial effects in patients with different kinds | Zhen Xiao Sun Qing Wen Ma Tian De Zhao Yu Lin Wei Guang Sheng Wang Jia Shi Li | 2000 | World Journal of Gastroenterology2000，6，2： | 31 |
| 17 | Anti-tumor activity of wogonin, an extract from Scutellaria baicalensis, through regulating different signaling pathways显示文摘Wogonin is a plant flavonoid compound extracted from Scutellaria baicalensis(Huang-Qin or Chinese skullcap) and has been studied thoroughly by many researchers till date for its anti-viral, anti-oxidant, anti-cancerous and neuro-protective properties. Numerous experiments conducted in vitro and in vivo have demonstrated wogonin's excellent tumor inhibitory properties. The anticancer mechanism of wogonin has been ascribed to modulation of various cell signaling pathways, including serine-threonine kinase Akt(also known as protein kinase B) and AMP-activated protein kinase(AMPK) pathways, p53-dependent/independent apoptosis, and inhibition of telomerase activity. Furthermore, wogonin also decreases DNA adduct formation with a carcinogenic compound 2-Aminofluorene and inhibits growth of drug resistant malignant cells and their migration and metastasis, without any side effects. Recently, newly synthesized wogonin derivatives have been developed with impressive anti-tumor activity. This review is the succinct appraisal of the pertinent articles on the mechanisms of anti-tumor properties of wogonin. We also summarize the potential of wogonin and its derivatives used alone or as an adjunct therapy for cancer treatment. Furthermore, pharmacokinetics and side effects of wogonin and its analogues have also been discussed. | Do Luong Huynh Neelesh Sharma Amit Kumar Singh Simrinder Singh Sodhi ZHANG Jiao-Jiao Raj Kumar Mongre Mrinmoy Ghosh Nameun Kim Yang Ho Park Dong Kee Jeong | 2017 | Chinese Journal of Natural Medicines2017，15，1： | 32 |
| 18 | Apoptosis and non-alcoholic fatty liver diseases显示文摘The number of patients with nonalcoholic fatty liver diseases(NAFLD) including nonalcoholic steatohepatitis(NASH), has been increasing. NASH causes cirrhosis and hepatocellular carcinoma(HCC) and is one of the most serious health problems in the world. The mechanism through which NASH progresses is still largely unknown. Activation of caspases, Bcl-2 family proteins, and c-Jun N-terminal kinase-induced hepatocyte apoptosis plays a role in the activation of NAFLD/NASH. Apoptotic hepatocytes stimulate immune cells and hepatic stellate cells toward the progression of fibrosis in the liver through the production of inflammasomes and cytokines. Abnormalities in glucose and lipid metabolism as well as microbiota accelerate these processes. The production of reactive oxygen species, oxidative stress, and endoplasmic reticulum stress is also involved. Cell death, including apoptosis, seems very important in the progression of NAFLD and NASH. Recently, inhibitors of apoptosis have been developed as drugs for the treatment of NASH and may prevent cirrhosis and HCC. Increased hepatocyte apoptosis may distinguish NASH from NAFLD, and the improvement of apoptosis could play a role in controlling the development of NASH. In this review, the association between apoptosis and NAFLD/NASH are discussed. This review could provide their knowledge, which plays a role in seeing the patients with NAFLD/NASH in daily clinical practice. | Tatsuo Kanda Shunichi Matsuoka Motomi Yamazaki Toshikatsu Shibata Kazushige Nirei Hiroshi Takahashi Tomohiro Kaneko Mariko Fujisawa Teruhisa Higuchi Hitomi Nakamura Naoki Matsumoto Hiroaki Yamagami Masahiro Ogawa Hiroo Imazu Kazumichi Kuroda Mitsuhiko Moriyama | 2018 | World Journal of Gastroenterology2018，24，25： | 32 |
| 19 | Targeting calcium signaling in cancer therapy显示文摘The intracellular calcium ions(Ca^(2+)) act as second messenger to regulate gene transcription,cell proliferation, migration and death. Accumulating evidences have demonstrated that intracellular Ca^(2+)homeostasis is altered in cancer cells and the alteration is involved in tumor initiation, angiogenesis,progression and metastasis. Targeting derailed Ca^(2+)signaling for cancer therapy has become an emerging research area. This review summarizes some important Ca^(2+)channels, transporters and Ca^(2+)-ATPases,which have been reported to be altered in human cancer patients. It discusses the current research effort toward evaluation of the blockers, inhibitors or regulators for Ca^(2+)channels/transporters or Ca^(2+)-ATPase pumps as anti-cancer drugs. This review is also aimed to stimulate interest in, and support for researchinto the understanding of cellular mechanisms underlying the regulation of Ca^(2+)signaling in different cancer cells, and to search for novel therapies to cure these malignancies by targeting Ca^(2+)channels or transporters. | Chaochu Cui Robert Merritt Liwu Fu Zui Pan | 2017 | Acta Pharmaceutica Sinica B2017，7，1： | 32 |
| 20 | Effect of hepatocyte apoptosis induced by TNF-α on acute severe hepatitis in mouse models显示文摘AIM To study the effect of hepatocyteapoptosis and necrosis induced by TNF-α on thepathogenesis of acute severe hepatitis(ASH).METHODS The model of ASH was prepared inD-galactosamine(GAIN)sensitized BALB/c miceby injection of either endotoxin(ET)or tumornecrosis factor-α(TNF-α).Morphologicalchanges of apoptotic hepatocytes were studiedby both light and electron microscope and in siteend labeling method(ISEL).Molecular biologicalchanges of DNA ladder were observed byelectrophoresis of extract from liver tissues.Biochemical changes were measured by alanineaminotransferase(ALT),asparticaminotransferase(AST)and TNF-α.The relationbetween apoptosis and necrosis was evaluatedsimultaneously.RESULTS The sequence of hepatocyteapoptosis,necrosis,and final death from ASHwas observed both in GAIN/ET and GAIN/TNF-agroup.Apoptosis was prominent at 3.5 h and 5 hafter injection of inducer,while necrosis becamedominant at 9 h after challenge.The appearanceof apoptosis was earlier in GAIN/TNF-α groupthan that in GAIN/ ET group.Pretreatment ofmice with antiTNF IgG1 may completely preventthe liver injury induced by GalN/ET.CONCLUSION TNF-α can cause liver damageby inducing hepatic apoptosis and necrosis inmice with endotoxemia. | Guo Qing Zang Xia Qiu Zhou Hong Yu Qing Xie Guo Ming Zhao Bin Wang Qing Guo Yue Qin Xiang Dan Liao Department of Infectious Diseases,Rujin Hospital,Shanghai Second Medical University,Shanghai 200025,China | 2000 | World Journal of Gastroenterology2000，6，5： | 30 |
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