Experimental study on effect of PKC and protein tyrosine kinase on cardiomyocyte apoptosis during ischemia/reperfusion in rat heart

LIU Xing-de; et al

doi:10.13406/j.cnki.cyxb.2000.01.007

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Experimental study on effect of PKC and protein tyrosine kinase on cardiomyocyte apoptosis during ischemia/reperfusion in rat heart

更新时间：2024-01-17

- Experimental study on effect of PKC and protein tyrosine kinase on cardiomyocyte apoptosis during ischemia/reperfusion in rat heart
- Journal of Chongqing Medical University Issue 1, Pages: 20-22(2000)
- 作者机构：
  
  重庆医科大学临床学院心内科,400016
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.2000.01.007
  CLC： R329.2
- Published：2000，
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[1]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(01):20-22.

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 (1):20-22(2000)
[1]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(01):20-22. DOI： 10.13406/j.cnki.cyxb.2000.01.007.

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 (1):20-22(2000) DOI： 10.13406/j.cnki.cyxb.2000.01.007.

摘要

为探讨缺血预适应（ＩｓｃｈｅｍｉｃＰｒｅｃｏｎｄｉｔｉｏｎｉｎｇ，ＩＰ）早期以及蛋白激酶Ｃ（ＰｒｏｔｅｉｎｋｉｎａｓｅＣ，ＰＫＣ）及蛋白酪氨酸激酶（ＰｒｏｔｅｉｎＴｙｒｏｓｉｎｅＫｉｎａｓｅ，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（Ｐ＜０．０１）；２、ＰＫＣ激动剂ＰＭＡ及ＰＴＫ激动剂ａｎｉｓｏｍｙｃｉｎ均能显著降低Ｉ／Ｒ心肌细胞凋亡（Ｐ＜０．０１）；３、ＰＫＣ抑制剂灯盏花素不能阻断ａｎｉｓｏｍｙｃｉｎ降低Ｉ／Ｒ心肌细胞凋亡的作用，而ＰＴＫ抑制剂ｌａｖｅｎｄｕｓｔｉｎＡ则能阻断ＰＭＡ的效应。上述研究显示：ＰＭＡ和ａｎｉｓｏｎｙｃｉｎ能模拟ＩＰ早期的抗Ｉ／Ｒ心肌细胞凋亡的作用；并提示在ＩＰ信息传递通路中ＰＴＫ位于ＰＫＣ的下游。

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.

关键词

蛋白激酶C酪氨酸激酶缺血再灌注心肌细胞凋亡

Keywords

Protein kinase CProtein tyrosine kinaseIschemia/reperfusion cardiomyocyte apoptosis

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