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Effectof Ginsenoside Re on Cardiomyocyte Apoptosis and Expression of Bcl-2/Bax Gene after Ischemia and Reperfusion in Rats 被引量:7
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作者 刘正湘 李志刚 刘晓春 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2002年第4期305-309,共5页
To observe the effectof ginsenoside Re on cardiomyocyte apoptosis and Bcl- 2 / Bax gene expression after ischemia (30 m in) and reperfusion (6 h) in rats and to elucidate the possible m echanism s of ginsenoside Re ... To observe the effectof ginsenoside Re on cardiomyocyte apoptosis and Bcl- 2 / Bax gene expression after ischemia (30 m in) and reperfusion (6 h) in rats and to elucidate the possible m echanism s of ginsenoside Re on inhibition of cardiom yocyte apoptosis,the ischem ia/ reperfusion heart m odel was established by ligating the left anterior descending branch of coronary artery in Wistar rats.The apoptotic cardiom yocytes were confirmed by transm ission electron m icroscopy and counted by in situ nick end labeling(TU NEL) method and lightm icroscopy.The m RNA and protein expression of Bcl- 2 and Bax genes were studied by in situ hybridization and im munohis- tochemical staining.Mean optical density (OD) value of the positive fields of m RNA and protein expression was quantitatively exam ined by im age analysis system.The results were as follows: (1) The apoptotic cardiomyocytes were found in ischemic fields in the ischem ia/ reperfusion group and weren't observed in the sham- operation group by transmission electron microscopy;(2 ) The num bers of the apoptotic cells were134.4 5± 4 5 .6 1/ field in the ischemia/ reperfusion group,and 90 .6 6± 19.2 2 / field in the ginsenoside Re- treated group.The differences was significant between two groups(P<0 .0 1) ;(3) Gene expression of Bcl- 2 and Bax were increased significantly in the is- chemia/ reperfusion group and ginsenoside Re- treated group when compared with the sham - opera- tion group.There was no significant difference in the gene expression of Bcl- 2 between the gin- senoside Re- treated group and ischemia/ reperfusion group(P>0 .0 5 ) ,but gene expression of Bax was decreased significantly in the ginsenoside Re- treated group as compared with the ischem ia/ reperfusion group(P<0 .0 1) .The ratio of Bcl- 2 / Bax was increased significantly in the ginseno- side Re- treated group when com pared with the ischem ia/ reperfusion group and sham- operation group.These findings suggest that m yocardial ischem ia- reperfusion can induce cardiom yocyte apoptosis,and ginsenoside Re can significantly inhibit cardiom yocyte apoptosis induced by ischemi- a- reperfusion in rats.It is concluded that ginsenoside Re inhibits cardiomyocyte apoptosis by in- hibiting expression of pro- apoptotic Bax gene and raising the ratio of Bcl- 2 / Bax. 展开更多
关键词 ginsenoside Re ischemia/ reperfusion cardiomyocyte apoptosis bcl- 2 / bax
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Intermittent hypoxia attenuates ischemia/reperfusion induced apoptosis in cardiac myocytes via regulating Bcl-2/Bax expression 被引量:47
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作者 JIANWENDONG HAIFENGZHU +3 位作者 WEIZHONGZHU HAILEIDING TIEMINMA ZHAONIANZHOU 《Cell Research》 SCIE CAS CSCD 2003年第5期385-391,共7页
Intermittent hypoxia has been shown to provide myocardial protection against ishemia/reperfusion-induced injury.Cardiac myocyte loss through apoptosis has been reported in ischemia/reperfusion injury. Our aim was to i... Intermittent hypoxia has been shown to provide myocardial protection against ishemia/reperfusion-induced injury.Cardiac myocyte loss through apoptosis has been reported in ischemia/reperfusion injury. Our aim was to investigate whether intermittent hypoxia could attenuate ischemia/reperfusion-induced apoptosis in cardiac myocytes and its potential mechanisms. Adult male Sprague-Dawley rats were exposed to hypoxia simulated 5000 m in a hypobaric chamber for 6 h/day, lasting 42 days. Normoxia group rats were kept under normoxic conditions. Isolated perfused hearts from both groups were subjected to 30 min of global ischemia followed by 60 min reperfusion.Incidence of apoptosis in cardiac myocytes was determined by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) and DNA agarose gel electrophoresis. Expressions of apoptosis related proteins,Bax and Bcl-2, in cytosolic and membrane fraction were detected by Western Blotting. After ischemia/reperfusion,enhanced recovery of cardiac function was observed in intermittent hypoxia hearts compared with normoxia group.Ischemia/reperfusion-induced apoptosis, as evidenced by TUNEL-positive nuclei and DNA fragmentation, was significantly reduced in intermittent hypoxia group compared with normoxia group. After ischemia/reperfusion,expression of Bax in both cytosolic and membrane fractions was decreased in intermittent hypoxia hearts compared with normoxia group. Although ischemia/reperfusion did not induce changes in the level of Bcl-2 expression in cytosolic fraction between intermittent hypoxia and normoxia groups, the expression of Bcl-2 in membrane fraction was upregulated in intermittent hypoxia group compared with normoxia group. These results indicated that the cardioprotection of intermittent hypoxia against ischemia/reperfusion injury appears to be in part due to reduce myocardial apoptosis. Intermittent hypoxia attenuated ischemia/reperfusion-induced apoptosis via increasing the ratio of Bcl-2/Bax, especially in membrane fraction. 展开更多
关键词 intermittent hypoxia apoptosis cardiac myocytes bax bcl-2.
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Correlation between expression of gastrin, somatostatin and cell apoptosis regulation gene bcl-2/bax in large intestine carcinoma 被引量:27
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作者 Jia-DingMao PeiWu +3 位作者 Xiang-HouXia Ji-QunHu Wen-BinHuang Guo-QiangXu 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第5期721-725,共5页
AIM: To explore the correlation between expression of somatostatin (SS), gastrin (GAS) and cell apoptosis regulation gene bcl-2/bax in large intestine carcinoma.METHODS: Sixty-two large intestine cancer tissue samples... AIM: To explore the correlation between expression of somatostatin (SS), gastrin (GAS) and cell apoptosis regulation gene bcl-2/bax in large intestine carcinoma.METHODS: Sixty-two large intestine cancer tissue samples were randomly and retrospectively selected from patients with large intestine carcinoma. Immunohistochemical staining for bcl-2, bax, GAS, SS was performed according to the standard streptavidin-biotin-peroxidase (S-P) method.According to the semi-quantitative integral evaluation, SS and GAS were divided into three groups as follows. Scores1-3 were defined as the low expression group, 4-8 as the intermediate expression group, 9-16 as the high expression group. Bax and bcl-2 protein expressions in different GAS and SS expression groups of large intestine carcinoma were assessed.RESULTS: The positive expression rate of bax had a prominent difference between SS and GAS high, intermediate and low expression groups (P<0.05, x2ss = 9.246; P<0.05,x2GAS = 6.981). The positive expression rate of bax in SS high (80.0%, 8/10) and intermediate (76.5%, 13/17)expression groups was higher than that in low expression group (40.0%, 14/35) (P<0.05, x2high vs low = 5.242; P<0.05,x2middle vs low = 6.097). The positive expression rate of bax in GAS high expression group (27.3%, 3/8) was lower than that in low expression group (69.4%, 25/36) (P<0.05,x2 = 4.594). However, bax expression in GAS intermediate expression group (46.7%, 7/15) was lower than that in low expression group, but not statistically significant. The positive expression rate of bcl-2 had a prominent difference between SS and GAS high, intermediate and low expression groups (P<0.05, x2ss = 7.178; P<0.05, x2GAS = 13.831). The positive expression rate of bcl-2 in GAS high (90.9%, 10/11)and intermediate (86.7%, 13/15) expression groups was higher than that in low expression group (44.4%, 16/36)(P<0.05,x2high vs low = 5.600; P<0.05, x2 middle vs low = 7.695).However, the positive expression rate of bcl-2 in SS high (40.0%, 4/10) and intermediate (47.1%, 8/9) expression groups was lower than that in low expression group (77.1%, 27/35)(P<0.05, x2 high vs low = 4.710; P<0.05, x2 middle vs low = 4.706).There was a significant positive correlation between the integral ratio of GAS to SS and the integral of bcl-2 (P<0.01,r=0.340). However, there was a negative correlation between the integral ratio of GAS to the SS and bax the integral of (P<0.05, r = -0.299).CONCLUSION: The regulation and control of gastrin,somatostatin in cell apoptosis of large intestine carcinoma may be directly related to the abnormal expression of bcl-2, bax. 展开更多
关键词 Large intestine carcinoma GASTRIN SOMATOSTATIN bcl-2 gene bax gene apoptosis
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Effects of Ethyl Pyruvate on Myocardial Apoptosis and Expression of Bcl-2 and Bax Proteins after Ischemia-reperfusion in Rats 被引量:26
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作者 郭家龙 张凯伦 +2 位作者 季艳梅 蒋雄刚 左顺庆 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2008年第3期281-283,共3页
In order to study the effects of ethyl pyruvate on cardiomyocyte apoptosis following ischemia/reperfusion (I/R) in vitro and the expression of Bcl-2 and Bax proteins, isolated rat hearts were perfused in a Langendor... In order to study the effects of ethyl pyruvate on cardiomyocyte apoptosis following ischemia/reperfusion (I/R) in vitro and the expression of Bcl-2 and Bax proteins, isolated rat hearts were perfused in a Langendorff model. Twenty-four rats were randomly divided into 3 groups (n=8 in each group): control group was perfused for 120 min. In the I/R group, after 30 min stabilization the injury was induced by 30 min global ischemia followed by 60 min reperfusion. Ethyl pyruvate (EP) group was set up with the same protocol as I/R group except that it was supplied with 2 mmol/L EP 15 rain before ischemia and throughout reperfusion. Myocardial malonaldehyde (MDA) content was measured. Myocardial apoptotic index (AI) was tested by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) method. The expression of anti-apoptotic protein Bcl-2 and pro-apoptotic protein Bax in cardiac myocytes was detected by immunohistochemistry. As compared with control group, the content of MDA, myocardial AI and the expression of Bcl-2, Bax proteins were increased significantly in I/R group, but the content of MDA, myocardial AI and the expression of Bax protein were decreased obviously and the expression of Bcl-2 protein was up-regulated in EP group (P〈0.05). These results demonstrate that EP could inhibit apoptosis of cardiac myocytes possibly via alleviating oxidative stress, up-regulating Bcl-2 and down-regulating Bax proteins. 展开更多
关键词 ethyl pyruvate myocardial reperfusion injury apoptosis bcl-2 protein bax protein
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Exogenous phosphatidylethanolamine induces apoptosis of human hepatoma HepG2 cells via the bcl-2/bax pathway 被引量:10
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作者 Yu Yao Chen Huang +7 位作者 Zong-Fang Li Ai-Ying Wang Li-Ying Liu Xiao-Ge Zhao Yu Luo Lei Ni Wang-Gang Zhang Tu-Sheng Song 《World Journal of Gastroenterology》 SCIE CAS CSCD 2009年第14期1751-1758,共8页
AIM: To investigate the signaling pathways implicated in phosphatidylethanolamine (PE)-induced apoptosis of human hepatoma HepG2 cells. METHODS: Inhibitory effects of PE on human hepatoma HepG2 cells were detected by ... AIM: To investigate the signaling pathways implicated in phosphatidylethanolamine (PE)-induced apoptosis of human hepatoma HepG2 cells. METHODS: Inhibitory effects of PE on human hepatoma HepG2 cells were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell cycle, apoptosis and mitochondrial transmembrane potential (ΔΨm) were analyzed by flow cytometry. Immunocytochemical assay and Western blotting were used to examine Bcl-2, Bax and caspase-3 protein levels in HepG2 cells treated with PE. RESULTS: PE inhibited the growth of HepG2 cells in a doseand timedependent manner. It did notaffect the cell cycle, but induced apoptosis. PE significantly decreased ΔΨm at 0.25, 0.5 and 1 mmol/L, respectively, suggesting that PE induces cell apoptosis by decreasing the mitochondrial transmembrane potential. The Bcl-2 expression level induced by different concentrations of PE was lower than that in control groups. However, the Bax expression level induced by PE was higher than that in the control group. Meanwhile, PE increased the caspase-3 expression in a doseand time-dependent manner. CONCLUSION: Exogenous PE induces apoptosis of human hepatoma HepG2 cells via the bcl-2/bax pathway. 展开更多
关键词 apoptosis bcl-2 bax Caspase-3 PHOSPHATIDYLETHANOLAMINE Human hepatoma HepG2 cell
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Effect of Hypoxic Preconditioning on Neural Cell Apoptosis and Expression of Bcl-2 and Bax in Cerebral Ischemia-Reperfusion in Rats 被引量:10
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作者 高晓群 常成 +2 位作者 段东晓 茹立强 殷光甫 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2006年第1期17-20,共4页
In order to investigate the protective effect of hypoxic preconditioning on the cerebral ischemia-reperfusion injury, the expression of Bcl-2 and Bax was detected by using immunohistochemical staining after 3 h cerebr... In order to investigate the protective effect of hypoxic preconditioning on the cerebral ischemia-reperfusion injury, the expression of Bcl-2 and Bax was detected by using immunohistochemical staining after 3 h cerebral ischemia followed by 1, 6, 12, 24 and 48 h reperfusion respectively in rats treated with or without hypoxic preconditioning before cerebral ischemia. In addition, the apoptosis of neural cells and the behavioral scores for neurological functions recovery were evaluated by TUNEL staining and "crawling method", respectively. Compared with control group (cerebral ischemia-reperfusion without hypoxic preconditioning), the expression of Bcl-2 was significantly increased, but that of Bax decreased in the hypoxic preconditioning group (cerebral ischemiareperfusion with hypoxie preconditioning), both P〈0.05. The pre-treatment with hypoxic preconditioning could reduce the apoptosis of neural cells and promote the neurological function recovery as compared to control group. It was suggested that hypoxic preconditioning may have protective effects on the cerebral ischemia-reperfusion injury by inhibiting the apoptosis of neural cells, increase the expression of Bcl-2 and decrease the expression of Bax. 展开更多
关键词 hypoxic preconditioning cerebral ischemia apoptosis bcl-2 bax
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Gambogic acid induces mitochondria-dependent apoptosis by modulation of Bcl-2 and Bax in mantle cell lymphoma JeKo-1 cells 被引量:18
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作者 Jingyan Xu Min Zhou +7 位作者 Jian Ouyang Jing Wang Qiguo Zhang Yong Xu Yueyi Xu Qian Zhang Xihui Xu Hui Zeng 《Chinese Journal of Cancer Research》 SCIE CAS CSCD 2013年第2期183-191,共9页
Objective: To study the mechanisms in gambogic acid (GA) -induced JeKo-1 human Mantle Cell Lymphoma cell apoptosis in vitro. Methods: The proliferation of GA-treated JeKo-1 cells was measured by CCK-8 assay and Ki... Objective: To study the mechanisms in gambogic acid (GA) -induced JeKo-1 human Mantle Cell Lymphoma cell apoptosis in vitro. Methods: The proliferation of GA-treated JeKo-1 cells was measured by CCK-8 assay and Ki-67 immunocytochemical detection. Apopt0sis, cell cycle and mitochondrial membrane potential were measured by flow cytometric analysis. Caspase-3, -8 and -9 were detected by colorimetric assay. Bcl-2 and Bax were analyzed by Western blotting. Results: GA inhibited cell growth in a time- and dose- dependent manner. GA induces apoptosis in JeKo- 1 cells but not in normal bone marrow cells, which was involved in reducing the membrane potential of mitochondria, activating caspases-3, -8 and -9 and decreasing the ratio of Bd-2 and Bax without cell cycle arresting. Conclusions: GA induced apoptosis in human MCL JeKo-1 cells by regulating Bcl-2/Bax and activating caspase-3, -8 and -9 via mitochondrial pathway without affecting cell cycle. 展开更多
关键词 Gambogic acid JeKo-1 cells cell cycle arrest apoptosis membrane potential of mitochondria caspase-3 CASPASE-8 caspase-9 bax bcl-2
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Mechanical stretch induces mitochondria-dependent apoptosis in neonatal rat cardiomyocytes and G_(2)/M accumulation in cardiac fibroblasts 被引量:6
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作者 XuDongLIAO XiaoHuiWANG +2 位作者 HaiJingJIN LanYingCHEN QuanCHEN 《Cell Research》 SCIE CAS CSCD 2004年第1期16-26,共11页
Heart remodeling is associated with the loss of cardiomyocytes and increase of fibrous tissue owing to abnormal mechanical load in a number of heart disease conditions. In present study, a well-described in vitro sust... Heart remodeling is associated with the loss of cardiomyocytes and increase of fibrous tissue owing to abnormal mechanical load in a number of heart disease conditions. In present study, a well-described in vitro sustained stretch model was employed to study mechanical stretch-induced responses in both neonatal cardiomyocytes and cardiac fibroblasts. Cardiomyocytes, but not cardiac fibroblasts, underwent mitochondria-dependent apoptosis as evidenced by cytochrome c (cyto c) and Smac/DIABLO release from mitochondria into cytosol accompanied by mitochondrial membrane potential (△ψ_m) reduction, indicative of mitochondrial permeability transition pore (PTP) opening. Cyclosporin A, an inhibitor of PTP, inhibited stretch-induced cyto c release, △ψ_m reduction and apoptosis, suggesting an important role of mitochondrial PTP in stretch-induced apoptosis. The stretch also resulted in increased expression of the pro-apoptotic Bcl-2 family proteins, including Bax and Bad, in cardiomyocytes, but not in fibroblasts. Bax was accumulated in mitochondria following stretch. Cell permeable Bid-BH3 peptide could induce and facilitate stretch-induced apoptosis and △ψ_m reduction in cardiomyocytes. These results suggest that Bcl-2 family proteins play an important role in coupling stretch signaling to mitochondrial death machinery, probably by targeting to PTP. Interestingly, the levels of p53 were increased at 12 h after stretch although we observed that Bax upregulation and apoptosis occurred as early as 1 h. Adenovirus delivered dominant negative p53 blocked Bax upregulation in cardiomyocytes but showed partial effect on preventing stretch-induced apoptosis, suggesting that p53 was only partially involved in mediating stretch-induced apoptosis. Furthermore, we showed that p21 was upregulated and cyclin B1 was downregulated only in cardiac fibroblasts, which may be associated with G_2/M accumulation in response to mechanical stretch. 展开更多
关键词 apoptosis mechanical stretch bcl-2 and its family proteins MITOCHONDRIA cardiomyocyte.
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Effects of genistein on neuronal apoptosis,and expression of Bcl-2 and Bax proteins in the hippocampus of ovariectomized rats 被引量:6
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作者 Yun Peng Bo Jiang +2 位作者 Huiling Wu Ruchun Dai Liming Tan 《Neural Regeneration Research》 SCIE CAS CSCD 2012年第36期2874-2881,共8页
Genistein is one of several isoflavones that has a structure similar to 17β-estradiol, has a strong antioxidant effect, and a high affinity to estrogen receptors. At 15 weeks after ovariectomy, the expression of Bcl-... Genistein is one of several isoflavones that has a structure similar to 17β-estradiol, has a strong antioxidant effect, and a high affinity to estrogen receptors. At 15 weeks after ovariectomy, the expression of Bcl-2 in the hippocampus of rats decreased and Bax expression increased, with an obvious upregulation of apoptosis. However, intraperitoneal injection of genistein or 17β-estradiol for 15 consecutive weeks from the second day after operation upregulated Bcl-2 protein expression downregulated Bax protein expression, and attenuated hippocampal neuron apoptosis. Our experimental findings indicate that long-term intervention with genistein can lead to a decrease in apoptosis in hippocampal neurons following ovadectomy, upregulate the expression of Bcl-2, and downregulate the expression of Bax. In addition, genistein and 17β-estradiol play equal anti-apoptotic and neuroprotective roles. 展开更多
关键词 ovariectomized model rats HIPPOCAMPUS apoptosis bcl-2 bax GENISTEIN 17Β-ESTRADIOL braininjury neural regeneration
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Simvastatin inhibits apoptosis of endothelial cells induced by sepsis through upregulating the expression of Bcl-2 and downregulating Bax 被引量:18
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作者 Hui Fu Qiao-sheng Wang +5 位作者 Qiong Luo Si Tan Hua Su Shi-lin Tang Zheng-liang Zhao Li-ping Huang 《World Journal of Emergency Medicine》 CAS 2014年第4期291-297,共7页
BACKGROUND: Many studies have showed that apoptosis of endothelial cells plays a curial role in the progress of sepsis. But the role of simvastatin in apoptosis of endothelial cells induced by sepsis is not clear. The... BACKGROUND: Many studies have showed that apoptosis of endothelial cells plays a curial role in the progress of sepsis. But the role of simvastatin in apoptosis of endothelial cells induced by sepsis is not clear. The present study aimed to investigate the role of simvastatin in apoptosis of endothelial cells induced by sepsis and its mechanism.METHODS: Human umbilical vein endothelial cells(HUVECs) were randomly divided into three groups: control group, sepsis serum intervention group(sepsis group) and simvastatin+sepsis serum intervention group(simvastatin group). After 24-hour incubation with corresponding culture medium, the relative growth rate of HUVECS in different groups was detected by MTT assay; the apoptosis of HUVECs was detected by Hoechst33258 assay and fl ow cytometry; and the expression of the Bcl-2 and Bax genes of HUVECs was detected by PCR.RESULTS: Compared with the sepsis group, HUVECs in the simvastatin group had a higher relative growth rate. Apoptotic HUVECs decreased significantly in the simvastatin group in comparison with the sepsis group. Expression of the Bcl-2 gene in HUVECs decreased obviously, but the expression of the Bax gene increased obviously after 24-hour incubation with sepsis serum; however, the expression of the Bcl-2 and Bax genes was just the opposite in the simvastatin group.CONCLUSIONS: Our study suggests that simvastatin can inhibit apoptosis of endothelial cells induced by sepsis through upregulating the expression of Bcl-2 and downregulating Bax. It may be one of the mechanisms for simvastatin to treat sepsis. 展开更多
关键词 SIMVASTATIN SEPSIS Endothelial cells apoptosis bcl-2 GENE bax GENE
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Propofol blocks apoptosis and Bcl-2 and Bax expression induced by hypoxia-reoxygenation in primary cultures of rat hippocampal astrocytes 被引量:3
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作者 Qing Li Juying Liu Long Zhou Chengming Qin 《Neural Regeneration Research》 SCIE CAS CSCD 2009年第7期518-522,共5页
BACKGROUND: Cerebral hippocampal astrocytes are more sensitive.to ischemic injury than neurons. Hypoxic-ischemic brain injury induces profound astrocyte apoptosis, and propofol may protect against astrocyte apoptosis... BACKGROUND: Cerebral hippocampal astrocytes are more sensitive.to ischemic injury than neurons. Hypoxic-ischemic brain injury induces profound astrocyte apoptosis, and propofol may protect against astrocyte apoptosis. OBJECTIVE: To verify the protective effects of propofol against astrocyte apoptosis and to investigate anti-apoptotic Bcl-2 and pro-apoptotic Bax expression in primary cultures of rat hippocampal astrocytes exposed to hypoxia-reoxygenation for different periods of time following propofol treatment. DESIGN, TIME, AND SETTING: In vitro neural immunocytochemistry was performed at the Central Laboratory of Yunyang Medical College between September 2007 and March 2008.MATERIALS: A total of 30 Wistar rats, aged 1-3 days, wJth equal numbers of males and females, were included for isolation and culture of .hippocampal astrocytes. METHODS: Hippocampal astrocytes were purified and cultured for 3 weeks and treated with four culture conditions: 50 μL Hank's solution (normal control); 0.2 mL/L Intralipid; 50 μL Hank's solution for 10 minutes followed by hypoxic incubation for 4 hours and normoxic incubation for 12, 24, 36, 48, 60 or 72 hours; propofol (250 μmol/L final) for 10 minutes followed by hypoxic incubation for 4 hours and normoxic incubation for 12, 24, 36, 48, 60 and 72 hours. MAIN OUTCOME MEASURES: (1) Morphologic changes in hippocampal astrocytes. (2) Levels of astrocyte apoptosis and Bcl-2 and Bax expression. RESULTS: Hypoxia and reoxygenation increased apoptosis over time, with Bcl-2 expression peaking at 24 hours and decreasing gradually (P 〈 0.01 ); Bax expression peaked at 72 hours (P 〈 0.01); the ratio of Bcl-2/Bax was 1.4, 0.8, and 0.6, respectively, at 24, 48 and 72 hours. Non-apoptotic astrocytes showed significant proliferation and swelling. Propofol treatment decreased apoptosis after hypoxia-reoxygenation (P 〈 0.01), as well as Bct-2 and Bax expression (P 〈 0.05, P 〈 0.01), with Bcl-2/Bax ratios of 1.6-1.8. Propofol treatmentalso blocked astrocyte proliferation and swelling. No apoptotic cells or Bcl-2/Bax expression was detected in astrocytes cultured in Hank's or Intralipid solution. CONCLUSION: Propofol protects astrocytes against injury caused by hypoxia and reoxygenation via a mechanism that involves maintaining high ratios of Bcl-2/Bax. 展开更多
关键词 PROPOFOL hippocampal astrocyte apoptosis hypoxia and re-oxygenation bcl-2 bax
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Brain-derived neurotrophic factor prevents beta-amyloid-induced apoptosis of pheochromocytoma cells by regulating Bax/Bcl-2 expression 被引量:2
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作者 Zhikun Sun Xingrong Ma +2 位作者 Hongqi Yang Jiahua Zhao Jiewen Zhang 《Neural Regeneration Research》 SCIE CAS CSCD 2012年第5期347-351,共5页
Brain-derived neurotrophic factor was utilized in the present study to treat cell injury models induced by aggregated β-amyloid(25 35). Methylthiazolyldiphenyl-tetrazolium bromide assay and western blot analysis sh... Brain-derived neurotrophic factor was utilized in the present study to treat cell injury models induced by aggregated β-amyloid(25 35). Methylthiazolyldiphenyl-tetrazolium bromide assay and western blot analysis showed that brain-derived neurotrophic factor provided neuroprotection against cellular apoptosis by suppressing the decline in β-amyloid(25 35)-induced cell activity and the increasing ratio of Bax/Bcl-2. After treating pheochromocytoma cells with tyrosine kinase receptor B receptor inhibitor K252a, brain-derived neurotrophic factor reverses the above- mentioned changes. The experimental findings suggested that brain-derived neurotrophic factor prevented β-amyloid peptide-induced cellular apoptosis by modulating Bax/Bcl-2 expression, and this effect was associated with binding to the specific tyrosine kinase receptor B receptor. 展开更多
关键词 Alzheimer's disease apoptosis β-amyloid peptide bax brain-derived neurotrophic factor bcl-2 tyrosine kinase receptor B
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Effect of compound preparation Tongqiao Jiannao capsules on neural cell apoptosis and Bcl-2 and Bax protein levels in a rat model of brain ischemia/reperfusion injury 被引量:1
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作者 Rui Wang Guanglai Li +1 位作者 Wei Wang Huanying Li 《Neural Regeneration Research》 SCIE CAS CSCD 2008年第8期871-874,共4页
BACKGROUND:Pharmacological studies have demonstrated that compound preparation Tongqiao Jiannao capsules composed of Zexie, Baizhu, Honghua, Danshen, and Shexiang can supplement qi, activate blood circulation, reliev... BACKGROUND:Pharmacological studies have demonstrated that compound preparation Tongqiao Jiannao capsules composed of Zexie, Baizhu, Honghua, Danshen, and Shexiang can supplement qi, activate blood circulation, relieve blood stasis, induce resuscitation for alleviating pain, relieve pain, and dilate blood vessels. OBJECTIVE: To observe the effects of Tongqiao Jiannao capsules on the levels of the anti-apoptotic protein Bcl-2 and the proapoptotic protein Bax, and verify the mechanism of action. DESIGN, TIME AND SETTING: Randomized, controlled animal experiment, performed in the Laboratory of Biochemistry and Molecular Biology, Shanxi Medical University between June 2001 and December 2002. MATERIALS: The right middle cerebral arteries of 24 healthy adult Sprague Dawley rats were occluded by the suture method. The primary Chinese herbal medicinal ingredients of Tongqiao Jiannao capsules are Zexie, Baizhu, Honghua, Danshen, and Shexiang, which were purchased from Shanxi Provincial Medicinal Material Company, China, and prepared into condensed granules in the Room for Chinese Herbal Medicine Preparation, Second Hospital, Shanxi Medical University. Bcl-2 and Bax immunohistochemical staining kits, a 3,3-diaminobenzidine(DAB) kit, and an in situ apoptosis detection kit were purchased from Wuhan Boster Bioengineering Co., Ltd., China. METHODS: Twenty-four rats were randomly and evenly divided into three groups: (1) sham-operated rats in which sutures were inserted and immediately pulled out; (2) Tongqiao Jiannao capsule-treated rats that were intragastrically administered 6.5 g/kg/d Tongqiao Jiannao capsule preparation for seven successive days prior to middle cerebral artery occlusion (MCAO); and (3) MCAO rats without any other treatments. MAIN OUTCOME MEASURES: The levels of neural cell apoptosis and Bcl-2 and Bax proteins at 24 hours post-surgery. RESULTS: In the MCAO group, the numbers of apoptotic cells and Bax-positive cells were significantly increased, while the numbers of Bcl-2-positive cells were slightly decreased compared with the sham-operated group. Bcl-2- and Bax-positive cells and apoptotic cells were primarily distributed in the ischemic penumbra. In the Tongqiao Jiannao capsule-treated group, neuronal apoptosis was inhibited, and the number of Bcl-2-positive cells was significantly increased (P 〈 0.01), while the number of Bax-positive cells was significantly decreased (P 〈 0.01), compared with the MCAO group. CONCLUSION: Tongqiao Jiannao capsules elevated Bcl-2 expression, lowered Bax expression, and inhibited cellular apoptosis during the process of cerebral ischemia/reperfusion injury. 展开更多
关键词 Tongqiao Jiannao capsules cerebral ischemia/reperfusion cellular apoptosis bcl-2 bax bcl-2/bax
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Effect of exogenous phosphocreatine on cardiomycytic apoptosis and expression of Bcl-2 and Bax after cardiopulmonary resuscitation in rats 被引量:1
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作者 Ping Yan Shou-quan Chen +6 位作者 Zhang-ping Li Jie Zhang Ji-ke Xue Wan-tie Wang Wei-jia Huang Jun-yan Cheng Hui-ping Li 《World Journal of Emergency Medicine》 SCIE CAS 2011年第4期291-295,共5页
BACKGROUND: Ischemia-reperfusion injury in the myocardium after cardiac arrest (CA)and cardiopulmonary resuscitation (CPR) is an important pathologic basis of post-cardiac arrestof syndrome (PCAS), and apoptosi... BACKGROUND: Ischemia-reperfusion injury in the myocardium after cardiac arrest (CA)and cardiopulmonary resuscitation (CPR) is an important pathologic basis of post-cardiac arrestof syndrome (PCAS), and apoptosis is one of the major mechanisms in myocardial ischemiareperfusioninjury. To lessen myocardial ischemia-reperfusion injury after cardiac arrest and CPR,it is important to reduce energy consumption and to increase energy supply in the myocardium.This study aimed to observe changes of cell apoptosis and expression of Bcl-2 and Bax proteinon the myocardium after CPR in rats, and the protective effects of different doses of exogenousphosphocreatine (creatine phosphate, CP) on them.METHODS: A total of 32 male adult Sprague-Dawley rats were randomly divided into 4 groups:control group (group A), CPR group (group B), low-dose CP group (group C, CP 0.5 g/kg at beginning ofCPR and 1.0 g/kg at 2 hours after CPR) and high-dose CP group (group D, CP 1.0 g/kg at beginning ofCPR and 2.0 g/kg at 2 hours after CPR). Cardiac arrest was induced by asphyxiation and CPR startedat 7 minutes after asphyxiation in groups B, C and D. Myocardium samples were taken at 24 hoursafter CPR. Cardiomycytic apoptosis was detected by the TdT-mediated dUTP-biotin nick end labeling(TUNEL) method. The expression of Bcl-2 and Bax protein was measured by immunohistochemistry.RESULTS: Cardiomyocytic apoptosis index (AI) and expression of Bcl-2 and Bax proteinincreased more significantly in groups B, C and D than in group A (P〈0.01), but Bcl-2/Bax ratiosignificantly decreased (P〈0.01). Cardiomyocytic AI and expression of Bcl-2 and Bax proteindecreased more significantly in groups C and D than in group B (P〈0.01), but Bcl-2/Bax ratioincreased more significantly (P〈0.01). Cardiomyocytic AI and expression of Bcl-2 and Bax proteindecreased more signifi cantly in group D than in group C (P〈0.05), but Bcl-2/Bax ratio increased moresignifi cantly (P〈0.05).CONCLUSION: Exogenous phosphocreatine, especially at a large dose, could inhibitcardiomyocytic apoptosis and alleviate myocardial injury after CPR in rats. 展开更多
关键词 CARDIOPULMONARY RESUSCITATION PHOSPHOCREATINE apoptosis bcl-2 bax TUNEL
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THE EXPRESSION AND CLINICAL VALUE OF APOPTOSIS CONTROL GENE Bcl-2 AND Bax IN BREAST CANCER
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作者 郑军 姚榛祥 张静 《Chinese Journal of Cancer Research》 SCIE CAS CSCD 1999年第3期221-223,共3页
Objective: To study the expression and clinical value of apoptosis control gene bcl-2 and bax in breast cancer. Methods: Protein bax and bcl-2 in 41 breast cancers obtained from operations in our hospital in 1996 were... Objective: To study the expression and clinical value of apoptosis control gene bcl-2 and bax in breast cancer. Methods: Protein bax and bcl-2 in 41 breast cancers obtained from operations in our hospital in 1996 were detected using ABC immunohistochemical stain assay and compared with 10 cases with normal breast tissues. Results: The positive rate of bax in normal breast tissue was 90% and in breast cancer was 59%, with a significant statistical difference between them (P<0.05), but there was no statistical difference in bcl-2 protein expression. Among the 41 breast cancer, the group with lymph node metastasis (21 cases) had obviously low bax expression (43%) and high bcl-2 expression (76%), showing significant difference to the group without lymph node metastasis (P<0.05). Conclusion: The antiapoptosis function of bcl-2 was stronger than bax in breast cancer. Protein bax and bcl-2 assay may be useful in understanding the biological behaviors of breast cancer. 展开更多
关键词 Breast cancer apoptosis control protein bax bcl-2 IMMUNOHISTOCHEMISTRY
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Total saponins in Rubus parvifolius L.induce lymphoma cells apoptosis through upregulated Bax/Fas and downregulated Bcl-2 in vivo and in vitro
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作者 Xiao-Feng Xu Ru-Bin Cheng +1 位作者 Xue-Jin Zhang Rui-Lan Gao 《Traditional Medicine Research》 2019年第2期99-108,共10页
Purpose:To investigate the effect of total saponins of Rubus parvifolius L.(TSRP)on lymphoma Raji cells and further discuss its mechanism.Methods:The model of nude mice bearing Raji cells was established,the volume,we... Purpose:To investigate the effect of total saponins of Rubus parvifolius L.(TSRP)on lymphoma Raji cells and further discuss its mechanism.Methods:The model of nude mice bearing Raji cells was established,the volume,weight and inhibition rate of the transplanted tumor were analyzed and compared after different concentrations of TSRP treatment.Cell apoptosis and expression of Bcl-2,Bax,Fas proteins were detected by TUNEL and immunohistochemiscal method respectively.Effects of TSRP on cell proliferation were tested with MTT assay in vitro.Cell apoptosis and expression of Caspase-9,Caspase-3,Bcl-2,Bax and Fas proteins were tested with DAPI staining and Western blot.Results:TSRP significantly reduced the volume and tumor weight of Raji subcutaneous transplanted tumor and induced the apoptosis of Raji cells in vivo.The tumor inhibition rate of high-dose(100 mg/kg)TSRP is 90.84%.The TUNEL test results show that the fluorescence intensity of the tumor issue treated with TSRP is significantly improved.Compared with the control group,the fluorescence intensity of high-concentration TSRP is 82.43 ± 7.81,which is significantly different(P<0.001).The results of immunohistochemistry test showed that the Bcl-2 expression of Raji cell treated with TSRP is obviously reduced,and Bax expression is obviously increased.Meanwhile,compared with that of control group,Fas expression is obviously reduced.MTT assay showed that TSRP can significantly inhibit proliferation of Raji cells with dose dependence.The inhibition rate of 400 μg/mL TSRP is 53.46 ± 4.90%(P<0.001).DAPI staining results showed that TSRP can significantly induce cell apoptosis.According to Western blot results,it is found that TSRP can significantly inhibit activity of Bcl-2 and increase Bax expression,and TSRP can also inhibit Fas expression.Meanwhile,expression of Caspase-9 and Caspase-3 is also increased.Conclusion:TSRP could inhibit the proliferation of lymphoma via induction of apoptosis in a time and dose-dependent manner.Apoptotic signaling induced by TSRP was characterized by up-regulating Bax,Fas and Caspase-8 protein expression,and down-regulating of Bcl-2 protein expression. 展开更多
关键词 Total SAPONINS of RUBUS parvifolius L. bcl-2 bax FAS apoptosis Lymphoma
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Effect of Wenxin granule on Bcl-2/Bax/Caspase apoptosis pathway gene expression in rats with myocardial infarction
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作者 Meng Lv Xiao-Di Ji +5 位作者 Ke-Ke Liu Ding Yang Li-Xia Lou Bo Nie Jiu-Li Zhao Ai-Ming Wu 《Journal of Hainan Medical University》 2022年第7期13-18,共6页
Objective:To explore the cardioprotective mechanism of Wenxin Granules regulating the expression of apoptosis-related genes in cardiomyocytes.Methods:A rat model of myocardial infarction was established and randomly d... Objective:To explore the cardioprotective mechanism of Wenxin Granules regulating the expression of apoptosis-related genes in cardiomyocytes.Methods:A rat model of myocardial infarction was established and randomly divided into model group,Wenxin granule low-dose group,Wenxin granule high-dose group,metoprolol group and sham operation group.the left ventricular end systole anterior wall thickness(LVAWs),end systole inner diameter(LVIDs),end systole posterior wall thickness(LVPWs),end-diastolic anterior wall thickness(LVAWd),end-diastolic inner diameter(LVIDd),end-diastolic posterior wall thickness(LVPWd)and left ventricular ejection fraction(LVEF)were detected by echocardiography in each group after 2 weeks of treatment.Hematoxylin eosin(HE)staining was used to observe the changes in the cardiac structure of rats in each group.Real-time PCR(Real-time PCR)was used to detect the relative expression of mammalian B-cell lymphoma-2(BCL-2),BCL-2 related X protein(BAX),Caspase-9(Caspase-9),and Caspase-3(Caspase-3)mRNA.TUNEL staining was used to detect changes in the apoptotic rate of rat cardiomyocytes in each group.Results:Compared with the sham operation group,the LVAWs,LVPWs,LVPWd and LVEF of the model group were significantly reduced(P<0.05,P<0.01),and LVIDs and LVIDd were significantly increased(P<0.05,P<0.01).Severe pathological ischemia injury of heart tissue.The relative expression of BCL-2 mRNA and the ratio of BCL-2/BAX in the model group were significantly reduced(P<0.01),while the relative expression of BAX,Caspase-9 and Caspase-3 mRNA was significantly increased(P<0.01).The apoptosis rate was significantly increased(P<0.01).In the low-dose and high-dose groups of Wenxin Granules and the Metoprolol group,LVAWs,LVPWs,LVPW d,and LVEF of rats in each administration group increased significantly(P<0.05,P<0.01),LVIDs,LVIDd was significantly reduced(P<0.05,P<0.01),the pathological damage of the heart tissue was improved,the expression of BCL-2 mRNA and the ratio of BCL-2/BAX were significantly increased(P<0.05,P<0.01),BAX,The expression of Caspase-9 and Caspase-3 mRNA was significantly reduced(P<0.05,P<0.01),and the apoptotic rate of myocardial cells was significantly reduced(P<0.01).Conclusion:Wenxin granule can play a cardioprotective role by regulating the gene expression of BCL-2/BAX/Caspase apoptosis pathway. 展开更多
关键词 Wenxin granule bcl-2/bax/Caspase apoptosis PATHWAY Miocardial infarction
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Differential expression of bcl-2 and bax genes during the E.coli-induced apoptosis of human U937 cells 被引量:1
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作者 JIA HE WANG YI JUN ZHOU +2 位作者 NA MA LI MIN ZHENG BAI YI CHEN 《Journal of Microbiology and Immunology》 2005年第4期270-273,共4页
To explore the role of bcl-2 and bax genes in the apoptosis of human U937 cells induced by E.coli, flow cytometry assay with annexinⅤ-FITC/PI double staining was used to determine the condition of apoptosis, and the ... To explore the role of bcl-2 and bax genes in the apoptosis of human U937 cells induced by E.coli, flow cytometry assay with annexinⅤ-FITC/PI double staining was used to determine the condition of apoptosis, and the expressions of mRNA of bcl-2 and bax genes were assayed with RT-PCR. It was found that the apoptosis of human U937 cells could be induced by E.coli at various concentration ratios between cells and bacteria for 30 min in a dose-dependent manner. The apoptotic rates at cell/bacteria ratios of 0, 1∶5, 1∶10, 1∶20, 1∶50 and 1∶100 were 3.16%±0.90%, 9.46%±0.84%, 17.90%±1.41%, 35.59%±3.76%, 38.35%±7.12% and 55.07%±5.82% respectively. Also, there was a tendency of alterations in the expression levels of bcl-2 and bax genes with an increased expression level of bax gene and a reduced expression level of bcl-2 gene. It is concluded that E.coli can induce apoptosis in human U937 cells with a down-regulated expression of Bcl-2 and an up-regulated expression of Bax, and this might be related to the induction of apoptosis of the infected cell. 展开更多
关键词 apoptosis E.coli U937 bcl- 2 bax
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Expression of Bcl-2 inhibited Fas-mediated apoptosis in human hepatocellular carcinoma BEL-7404 cells 被引量:29
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作者 CHANGYUNCHAO YONGHUAXU 《Cell Research》 SCIE CAS CSCD 2000年第3期233-242,共10页
Apoptosis plays an important role in embryonic development, tissue remodeling, immune regulation and tumor regression. Two groups of molecules (Bcl-2 family and "Death factor" family) are involved in regulat... Apoptosis plays an important role in embryonic development, tissue remodeling, immune regulation and tumor regression. Two groups of molecules (Bcl-2 family and "Death factor" family) are involved in regulating apoptosis. In order to know about the effect of Bcl-2 on apoptosis induced by Fas, a typical member of "Death factor" family, the transfection experiments with expression vectors pcDNA3-fl and pcDNA3-bcl-2 were performed in BEL-7404 cells, a human hepatocellular carcinoma cell line which expresses endogenous Fas, but not FasL and Bcl-2. The data showed that the expression of FasL in pcDNA3-fl transfected hepatoma cells obviously induced the apoptosis of the cells. However, the overexpression of Bcl-2 in pcDNA3-bcl-2 transfected 7404/b-16 cells counteracted pcDNA3-fl transient transfection mediated apoptosis. Further study by cotransfection experiments indicated that Bid but not Bax (both were pro-apoptotic proteins of Bcl-2 family) blocked the inhibitory effect of Bcl-2 on Fas-mediated apoptosis. These results suggested that Fas-mediated apoptosis in human hepatoma cells is possibly regulated by Bcl-2 family proteins via mitochondria pathway. 展开更多
关键词 apoptosis FASL bcl-2 BID bax human hepa- tocellular carcinoma cells.
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急性心肌梗死晚期再灌注后心肌细胞凋亡与Bcl-2、Bax蛋白表达的研究 被引量:17
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作者 屈朝法 马礼坤 +1 位作者 徐少东 吴学平 《中国病理生理杂志》 CAS CSCD 北大核心 2007年第4期656-659,共4页
目的:探讨犬急性心肌梗死后晚期再灌注对梗死周边缺血区心肌细胞凋亡及凋亡相关蛋白Bcl-2、Bax表达的影响。方法:健康成年杂交犬28只,全麻下常规开胸暴露冠状动脉后随机分为3组:假手术组(n=8),急性心肌梗死组(n=10)、晚期再灌注组(n=10... 目的:探讨犬急性心肌梗死后晚期再灌注对梗死周边缺血区心肌细胞凋亡及凋亡相关蛋白Bcl-2、Bax表达的影响。方法:健康成年杂交犬28只,全麻下常规开胸暴露冠状动脉后随机分为3组:假手术组(n=8),急性心肌梗死组(n=10)、晚期再灌注组(n=10)。假手术组仅行左冠状动脉前降支下穿过丝线而不结扎冠状动脉,急性心肌梗死组行左冠状动脉前降支高位永久结扎,晚期再灌注组在高位结扎左冠状动脉前降支6 h后松解结扎线予以再灌注6 h。共有23只犬模型制作成功。各组犬均于术后12 h处死,采集心肌标本。使用TUNEL法检测心肌细胞凋亡,免疫组化染色和Western blotting蛋白印迹分析Bcl-2、Bax在心肌细胞中表达情况。结果:晚期再灌注组心肌细胞凋亡数较急性心肌梗死组明显减少(P<0.05),但两组心肌细胞凋亡数均高于假手术组(P<0.01)。与假手术组相比,急性心肌梗死组和晚期再灌注组Bcl-2蛋白的表达均升高(P<0.01),其中在晚期再灌注组的表达略多于急性心肌梗死组,但无显著差异(P>0.05)。Bax蛋白在晚期再灌注组的表达高于假手术组(P<0.01),但低于急性心肌梗死组(P<0.05)。结论:急性心肌梗死后晚期再灌注可以减少梗死周边缺血区心肌细胞凋亡,其机制可能与心肌细胞表达Bax蛋白减少有关。 展开更多
关键词 心肌梗死 再灌注 心肌细胞 细胞凋亡 蛋白质bcl-2 蛋白质bax
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