依那普利干预对缺血-再灌注大鼠模型心肌细胞凋亡Bcl-2和Bax基因蛋白表达的影响

目的探讨依那普利干预对缺血再灌注大鼠模型心肌细胞凋亡Bcl-2和Bax基因蛋白表达的影响。方法雄性Wistar大鼠45只,随机分成3组:①缺血-再灌注(I/R)组15只,结扎左冠状动脉45min,松解4h,结扎前15min以及再灌注1h分别静脉注射生理盐水2ml/kg。②依那普利组(L)组15只:结扎左冠状45min,松解4h,结扎前15min以及再灌注1h分别静脉注射依那普利10mg/kg(依那普利以5mg/kg溶于生理盐水)。③假手术(C)组15只,冠状动脉下穿线不结扎,持续4.75h股静脉注射生理盐水2ml/kg。于实验结束时,取出心脏于4%多聚甲醛固定、石蜡包埋切片,按TUNEL法检测凋亡细胞,以S-P免疫组化法检测Bcl-2和Bax基因蛋白表达。结果①I/R组和L组标本中分别有13例和11例心肌细胞发生凋亡,L组凋亡细胞百分数较I/R组明显减少,差异具有高度显著性(P<0.05)。C组15例样本中12例均未检测到TUNEL阳性细胞。②L组Bcl-2表达较I/R组和C组均增强,L组Bax阳性心肌细胞较I/R组明显减少(P<0.05)。结论缺血-再灌注心肌细胞存在明显的凋亡现象,且受Bax蛋白与Bcl-2基因蛋白下调影响,Bax蛋白与Bcl-2蛋白共同调节心肌细胞凋亡,依那普利干预可诱导心肌细胞表达Bcl-2,减少心肌细胞凋亡。

Effect of Enalapril on expression of cadiocyte apoptosis Bcl-2 and Bax in rat model with ischemia-reperfusion

Objective To study the effect of Enalapril on expression of cadiocyte apoptosis Bcl-2 and Bax protein in different rats model with ischemia-reperfusion (I-R). Methods Forty-five male Wistar rats was divided into three groups by random, such as deligation auricular artery for 45min and unroll for 4h and intravenous injection NS with 2ml/kg before deligation for 15min and after reperfusion for 1h in I-R group; deligation auricular artery for 45min and unroll for 4h and intravenous injection Enalapril with 10mg/kg before deligation for 15min and after reperfusion for 1h in Enalapril group(L); without deligation auricular artery for 4.75h and vena femoralis injection NS with 2ml/kg in control group (C). The biopsy heart tissue with 4% formalin fixation and their chips with paraffin imbedding were made after experiment, and their apoptosis and Bcl-2 and Bax protein were detected by TUNEL and S-P immunohistochemical method, respectively. Results The apoptosis rate was lower in L group(11) than that in I-R group(13) (P<0.05). Without TUNEL positive cells were detected out in 12 of 15 samples in control group. The higher level of Bcl-2 and lower level of Bax were expressed in L group than those in I/R and control group (P<0.05). Conclusion Apoptosis can be expressed in cadiocytes with ischemia-reperfusion and can be down-regulated by Bcl-2 and Bax protein. The level of Bcl-2 in Cadiocytes can be induced by Enalapril so that cadiocyte apoptosis would decrease.