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目的观察热休克预处理对大鼠缺血再灌注损伤心肌细胞凋亡表达的影响。方法成年雌性Wistar大鼠(n=40)随机分3组。热休克组高热处理致肛温达(42±0.5)℃15min,24h后热休克组及对照组结扎LAD1h,再灌注2h,假手术组不结扎LAD。测血清CK-MB,心梗范围,Bax、Bcl-2及凋亡细胞。结果热休克组HSP70高于另两组(P<0.05),另两组比较差别无统计学意义(P>0.05);热休克组心梗范围、血清CK-MB、凋亡细胞及Bax均少于对照组(P<0.05),两组Bcl-2差别无统计学意义(P>0.05)。结论热休克预处理可抑制心肌缺血再灌注诱导的心肌细胞凋亡,抑制Bax的表达使Bax/Bcl-2比值下降是其机制之一。
Objective To observe the effect of heat shock preconditioning on myocardial cell apoptosis during ischemia / reperfusion injury in rats. Methods Adult female Wistar rats (n = 40) were randomly divided into 3 groups. In the heat shock group, the rectal temperature reached (42 ± 0.5) ℃ for 15 min after heat treatment. LAD1h was ligated in the heat shock group and the control group 24h later, and the LAD was reperfused for 2h in the sham operation group. Serum CK-MB, myocardial infarct size, Bax, Bcl-2 and apoptotic cells. Results Heat shock group HSP70 higher than the other two groups (P <0.05), the other two groups was no significant difference (P> 0.05); heat shock group myocardial infarction range, serum CK-MB, apoptotic cells and Bax are less In the control group (P <0.05), there was no significant difference between the two groups (P> 0.05). Conclusion Heat shock preconditioning can inhibit myocardial ischemia-reperfusion-induced cardiomyocyte apoptosis, and decrease the ratio of Bax / Bcl-2 by inhibiting the expression of Bax is one of the mechanisms.