期刊文献+

Caspase-3特异性抑制剂对缺血再灌注损伤诱导的大鼠心肌细胞凋亡的作用 被引量:9

Caspase-3 Inhibitor Reduces Apoptosis in Ischemic and Reperfused Myocardium of SD Rat
下载PDF
导出
摘要 目的:探讨caspase-3特异性抑制剂在大鼠缺血再灌注损伤诱导心肌细胞凋亡中的作用。方法:SD大鼠36只,随机分为3组:对照组、I/R3h组和抑制剂组。应用TUNEL法及流式细胞仪分析心肌细胞凋亡的变化,借助caspase-3荧光分析试剂盒,荧光比色法,检测心肌细胞凋亡过程中caspase-3活性的变化。结果:TUNEL及流式细胞仪分析显示caspase-3抑制剂组的AI值和细胞凋亡百分率分别为(4.48±0.98)%,(6.42±1.00)%;与I/R3h组[(18.33%±1.71)%,(29.88±3.74%)]相比明显降低并有显著差异(P<0.01)。caspase-3活性检测显示caspase-3抑制剂组的caspase-3活性明显降低,比I/R3h组降低了45.67%(P<0.01)。结论:caspase-3抑制剂能明显抑制心肌缺血再灌注后的心肌细胞凋亡。caspase-3抑制剂能明显抑制心肌缺血再灌注后的心肌caspase-3蛋白酶活性。 Objective:To investigate the significance of caspase-3 inhibitor in myocyte cell apoptosis induced by myocardial ischemia and reperfusion. Methods:Thirty-six SD rats were divided randomly into three groups, Control group, I/R3h group and caspase-3 inhibitor group. Myocyte cell apoptosis was detected by TUNEL and flow cytometry. The caspase-3 activity was detected by caspase-3 fluorescent assay kit. Results: TUNEL methlod and flow cytometry analysis showed that apoptosis indexes and the percentage of apoptosis cells in caspase-3 inhibitor was (4.48 ± 0.98) % and (6.42% ± 1.00) % respectively, and compared with the I/R3h group [(18.33 ± 1.71) %, (29. 88 ± 3. 74) %] were significantly lower(P〈20.01 ). Caspase-3 activity analysis showed that caspase-3 activity in caspase-3 inhibitor group was reduced 45.67% relative to I/R3h group. Conclusion: Caspase-3 inhibitor can efficiently inhibit myocyte cell apoptosis induced by myocardial ischemia and reperfusion. Caspase-3 inhibitor can efficiently inhibit activity of easpase-3 in cardiomyocytes after ischemia and reperfusion.
出处 《中国临床医学》 2009年第1期12-15,共4页 Chinese Journal of Clinical Medicine
基金 上海市重点学科建设项目(项目编号:B116)
关键词 大鼠 缺血 心肌细胞 调亡 Rat Ischmia Mycocyte Apoptosis
  • 相关文献

参考文献11

  • 1Gottlieb RA, Burleson KO, Kloner RP, et al. Reperfusion injury induces apoptosis in rabbit cardiomyocytes[J]. J Clin Invest, 1994,94: 1621-1628.
  • 2Freude B, Masters T N, Robicsek F, et al. Apoptosis is initiated by myocardial ischemia and executed during reperfusion[J]. J Mol Cell Cardiol,2000,32(2) : 197-208.
  • 3Stennieke HR, Ryan CA, Salvesen GS. Reprieval from execution: the molecular basis of easpase inhibition[J]. Trends Biochem Sci,2002,27: 94-101.
  • 4徐德民,赵强,陈安清,赵军,郑世营.缺氧诱导离体心肌细胞凋亡的动物实验研究[J].中国临床医学,2004,11(5):714-716. 被引量:4
  • 5徐德民,赵强,夏利民,赵军,郑世营.缺血再灌注损伤诱导大鼠心肌细胞凋亡的实验研究[J].中国临床医学,2006,13(4):549-551. 被引量:5
  • 6Searabelli T, Stephanou A, Rayment N, et al. Apoptosis of endothelial cells precedes myocyte cell apoptosis in Ischemia/ Reperfusion iniury[J]. Circulation,2001,104(3):253-258.
  • 7Stennieke HR, Ryan CA, Salvesen GS. Reprieval from execution: the molecular basis of easpase inhibition[J]. Trends Biochem Sci,2002,27 : 94-101.
  • 8Kim KS, Yoon ST, Li J, et al. Disc degeneration in the rabbit: a biochemical and radiological comparison between four disc injury models[J]. Spine, 2005,30( 1 ) :30-37.
  • 9赵军,郑世营,顾振纶,杨吉成,盛伟华.Caspase抑制剂对缺氧诱导的心肌细胞凋亡及相关基因表达的影响[J].苏州大学学报(医学版),2007,27(4):510-513. 被引量:7
  • 10Yaoita H, Ogawa K, Maehara K, et al. Apoptosis in relevant clinical situations: contribution of apoptosis in myocardial infarction[J]. Cardiovasc Res,2000,45:630-641.

二级参考文献33

  • 1赵军,郑世营,顾振纶,茅彩萍,杨吉成,盛伟华.Caspase-3特异性抑制剂对缺氧诱导鼠心肌细胞凋亡的影响[J].中华实验外科杂志,2004,21(9):1037-1039. 被引量:14
  • 2徐德民,赵强,陈安清,赵军,郑世营.缺氧诱导离体心肌细胞凋亡的动物实验研究[J].中国临床医学,2004,11(5):714-716. 被引量:4
  • 3赵军,徐德民,赵强,郑世营,顾振纶,茅彩萍,杨吉成,盛伟华.缺氧对心肌细胞DNA链损伤的体外实验研究[J].中国临床医学,2004,11(5):723-726. 被引量:2
  • 4[1]Currie A R,Kerr J F, Wyllie A H. Apoptosis: a basic biological phenomenon with wide- ranging Implications In tissue kinetics.Br J Cancer,1972,26:239~257.
  • 5[2]Matoba S, Tatumi T, Keira N, Cardioprotective effect of an giotensin - converting enzyme inhibition against Hypoxia/Reoxygenation injury in cultured rat cardiac myocytes. Circulation,1999,99: 817~822.
  • 6[3]Meier P, Finch A, Evan G. Apoptosis In development. Nature,2000,407: 796~801.
  • 7[4]Kang P M, Haunstetter A, Aoki H, et al. Morphological and molecular characterization of adult cardiomyocyte apoptosis dur ing hypoxia and reoxygenation. Circ Res, 2000, 87(2): 118~125.
  • 8[5]Hasenfuss G. Animal models of human cardiovascular disease,heart failture and hypertrophy. 1998, Cardiovasc Res, 39: 60 ~76.
  • 9[6]Malhotra R, Brosius FCⅢ. Glucose uptake and glycolysis reduce hypoxia - induced apoptosis in cultured neonatal rat cardiac myocytes. J Biol Chem, 1999,274:12567~12575.
  • 10[7]Moissac. DD, Gurevich RM, Zheng H, et al. Caspase activation and Mitochondrial cytochrome c release during hypoxiamediated apoptosis of adult ventricular myocytes. J Mol Cell Cardiol, 2000, 32: 53~63.

共引文献14

同被引文献108

引证文献9

二级引证文献138

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部