摘要
目的:通过观察高血压对大鼠脑缺血再灌注后神经功能和细胞凋亡的影响,探讨高血压加重缺血性脑损伤的机制。方法:将Wistar雄性大鼠随机分为肾性高血压缺血再灌注组(HIR),正常血压缺血再灌注组(IR)和假手术组(N),采用大脑中动脉线栓法造成大脑缺血再灌注模型,缺血时间为2h,再灌注24h。进行神经功能评分后取脑,采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:正常血压缺血再灌注组神经功能评分低于肾性高血压缺血再灌注组(P<0.05)。肾性高血压缺血再灌注组与正常血压缺血再灌注组比较,bcl-2表达明显减少(P<0.05),Bax表达明显增多(P<0.05),神经细胞凋亡明显增多(P<0.05)。结论:高血压通过增加Bax表达、抑制bcl-2表达,促进脑细胞凋亡,加重缺血再灌注后脑损伤。
Objective: To study the effects of hypertension on apoptosis of cell in rats with focal cerebral ischemia-reperfusion. Methods: Wistar male rats were divided randomly into hypertension ischemia and reperfusion group(HIR), normaltension ischemia and reperfusion group(IR) and sham-operated group(N). The focal cerebral ischemia model was established in Wistar rats by MCAO for 2h and reperfusion for 24h,then, neurological evaluation was carried out and the expression of bcl-2 and Bax were measured by immunohistochemistry. The apoptosis of cell was analyzed by TUNEL. Results: As compared with HIR,the neurological evaluation of IR was lower (P〈0.05). and the expression of Bax were higher and the expression of bcl-2 were lower in IR (P〈0. 05). Conclusion: Hypertension can inhibits the expression of bcl-2,and upregulate the expression of Bax in rats with focal cerebral ischemia-reperfusion.
出处
《陕西医学杂志》
CAS
北大核心
2008年第5期522-524,F0003,共4页
Shaanxi Medical Journal
基金
遵义医学院科技启动基金项目(2006)第12号