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（英文）

Influence of inhibiting p38MAPK on TNF-α expression and myocardial cell apoptosis in rats with ischemia/reperfusion injury

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刘组,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[(4.1 5±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。

Objective： To explore influence of p38 mitogen-activated protein kinase （p38MAPK） inhibitor on myocardial cell apoptosis and expression of tumor necrosis factor （TNF） -α in rats with ischemia/reperfusion （I/R） injury. Methods： According to number talde method, a total of 30 SD rats were randomly and equally divided into blank control group, I/R group and inhibitor group, p38MAPK mRNA expression, TNF-α level and myocardial cell apoptotic rate were measured, compared and analyzed among three groups. Results： Compared with blank control group, there were significant increase in TNF-αlevel [ （3.68±0.16） μg/L vs. （5.02±0.09） μg/L], p38MAPK mRNA expression [ （1.76±0.46） vs. （2.35±0.02）] and myocardial cell apoptotic rate [- （3. 51±0.40） % vs. - （1.8±0.23） %], P = 0. 001 all in I/R group. Compared with I/R group, there were significant decrease in p38MAPK mRNA expression （2.09±0.16）, TNF-α level [ （4.15±0.11） μg/L] and myocardial cell apoptotic rate [- （2.9±0.50） %] in inhibitor group, P=0. 001 all. Conclusion： Inhibition of p38 mitogen-activated protein kinase expression in myocardium of rats can decrease production of tumor necrosis factor-α and myocardial cell apoptosis, then relieve ischemia/ reperfusion injury of myocardial cells.