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蛋白激酶C和蛋白酪氨酸激酶活性对缺血再灌注心肌细胞凋亡影响的实验研究
引用本文:刘兴德,陈运贞.蛋白激酶C和蛋白酪氨酸激酶活性对缺血再灌注心肌细胞凋亡影响的实验研究[J].重庆医科大学学报,2000,25(1):20-22.
作者姓名:刘兴德  陈运贞
作者单位:重庆医科大学临床学院心内科 400016
摘    要:为探讨缺血预适应(Ischemic Preconditioning,IP)早期以及蛋白激酶C(Protein Kinase C,PKC)及蛋白酷氨酸激酶(Peotein Tyrosine Kinase,PTK)激动剂和抑制剂对缺血再灌注(I/R)心肌细胞凋亡的影响以及IP效能发挥通路中央PKC和PTK的关系。用TUNEL法检测I/R心肌细胞凋亡。结果显示:1、IP早期能显著降低I/R心肌细胞凋亡(

关 键 词:蛋白激酶C  酷氨酸激酶  细胞凋亡  心肌缺血
文章编号:0253-3626(2000)01-0020-03
修稿时间:1999年2月25日

Experimental study on effect of PKC and protein tyrosine kinase on cardiomyocyte apoptosis during ischemia / reperfusion in rat heart
LIU Xing-de,et al.Experimental study on effect of PKC and protein tyrosine kinase on cardiomyocyte apoptosis during ischemia / reperfusion in rat heart[J].Journal of Chongqing Medical University,2000,25(1):20-22.
Authors:LIU Xing-de  
Abstract:The purpose of this study was to use the TUNEL method for datecting I/R cardiomyocyte apoptosis to investigate the effect of ischemic preconditioning(IP),the activators of protein kinase C(PKC) and protein tyrosine kinase(PTK) on ischemia/reperfusion(I/R) cardiomyocyte apoptosis,and the relationship betWeen PKC and PTK for IPs anti-apoptosis effect in rat hearts.The results showed that:(1)IP could reduce MR cardiomyocyte apoptosis significantly (P<0.01);(2)PMA,the activator of PKC,and anisomycin,the activator of PTK,could also reduce I/R anisomycins anti-apoptosis during MR,and lavendustin A,the inhibitor of PTK,could block the effect of PMAs anti -apoptosis during I/R.These data suggest both PMA and anisomycin could mimic IPs anti-apoptosis effect during I/ R;PTK seems to be downstream of PKC for IPs anti-apoptosis effect during im injury in rat hearts.
Keywords:Protein kinase C  Protein tyrosine kinase  Ischemia/reperfusion cardiomyocyte apoptosis
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