ACEI对肾性高血压大鼠脑缺血再灌注后细胞凋亡的影响

Effects of ACEI on cell apoptosis in renal hypertension rats with focal cerebral ischemia-reperfusion

目的观察血管紧张素转化酶抑制剂(ACEI)对肾性高血压大鼠脑缺血再灌注后神经功能和细胞凋亡的影响,探讨ACEI的脑保护机制。方法采用狭窄肾动脉方法建立肾性高血压大鼠模型,随机分依那普利组(A组)和高血压缺血再灌注组(B组);正常血压组分为假手术组(C组)和缺血再灌注组(D组)。用线栓法造成大脑缺血再灌注模型,缺血时间为2h,再灌注时间22h。用免疫组织化学技术检测脑组织bcl-2、bax的表达,TUNEL法检测细胞凋亡。结果(1)脑缺血再灌注后神经功能评分:A组神经功能评分较B组和D组降低(P<0.05,);D组神经功能评分低于B组(P<0.05)。(2)A组与B组和D组比较bcl-2表达明显增多(P<0.05),bax表达显著降低(P<0.05),神经细胞凋亡明显减少(P<0.05);B组与D组比较,bcl-2表达明显降低(P<0.05),bax表达明显增加(P<0.05),而神经细胞凋亡明显增多(P<0.05)。结论ACEI明显改善局灶性脑缺血大鼠的神经功能,减少神经细胞凋亡,上调脑组织bcl-2表达,抑制bax表达,提示对脑缺血再灌注损伤有脑保护作用。

Objective To study the effects of ACEI（enalapril） on apoptosis of cell in renal hypertension rats with focal cerebral isehemia-reperfusion. Methods Renal hypertension rats were divided randomly into Enalapril group（A） and hypertension ischemic reperfusion group（B）. Normaltension group were dividing into sham-operated group（C） and normaltension ischemia and reperfusion group（D）. The focal cerebral isehemia model was established in Wistar rats by using the method of thread inserting left middle cerebral artery occlusion（MCAO） for 2h, then reperfusion 22h. The expression of bcl-2 and bax were measured by immunohistoehemistry. The apoptosis of cell was analyzed by TDT-mediated dUTP-bioten nick end labeling（TUNEL）. Results Compared with B and D, the neurological evaluation of A was lower（P〈0.05）. As compared with B,the neurological evaluation of D was lower （P〈0.05）. Compared with B and D,the expreesion of bcl-2 were higher and the expression of bax and the number of apoptosis were lower in A（P〈0.05）. Compared with B,the expression of bcl-2 was higher and the expression of bax and the number of apoptosiscells were fewer in D（P〈0.05）. Conclusion ACEI （Enalapril） can improve the neurological function and upregulate the expression of bcl-2,inhibit the expression of bax,and decrease the number of apoptosis in rats with focal cerebral ischemia-reperfusion.