抑制p38MAPK对大鼠缺血再灌注损伤心肌中TNF-α表达及细胞凋亡的影响
Chinese Journal of Cardiovascular Rehabilitation Medicine(2013)
Abstract
目的:探讨p38丝裂原活化蛋白激酶(p38MAPK)抑制剂对缺血再灌注损伤大鼠心肌细胞凋亡和肿瘤坏死因子-α(TNF-α)表达的影响.方法:将30只SD大鼠按随机数字法随机均分为空白对照组、缺血再灌注组和抑制剂组,各10只.检测各组p38MAPK mRNA表达,TNF-α水平及心肌细胞凋亡率,并进行比较分析.结果:与空白对照组比较,缺血再灌注组TNF-α[(3.68±0.16) μg/L比(5.02±0.09)μg/L]、p38MAPK mRNA的表达[(1.76±0.46)比(2.35±0.02)]和心肌细胞凋亡率[-(3.51±0.40)%比-(1.8±0.23)%]显著升高(P均=0.001).抑制剂组p38MAPK mRNA的表达[(2.09±0.16)]、TNF-α水平[(4.15±0.11)μg/L]及心肌细胞凋亡[-(2.9±0.50)%]均较缺血再灌注组显著降低(P均=0.001).结论:通过抑制大鼠心肌p38丝裂原活化蛋白激酶的表达能减少肿瘤坏死因子-α的生成,减少心肌细胞凋亡,进而减轻心肌细胞缺血再灌注损伤.
MoreKey words
Myocardium,Reperfusion injury,p38 mitogen-activated protein kinases
AI Read Science
Must-Reading Tree
Example
![](https://originalfileserver.aminer.cn/sys/aminer/pubs/mrt_preview.jpeg)
Generate MRT to find the research sequence of this paper
Chat Paper
Summary is being generated by the instructions you defined