低分子肝素对大鼠脑局灶性缺血再灌注后Bcl-2,Bax表达的影响及保护作用

目的:观察低分子肝素对大鼠脑缺血再灌注后不同时间点Bcl-2,Bax表达的影响及保护作用. 方法:①选用雄性SD大鼠54只,体质量280～330 g. 应用随机数字表法将大鼠分为3组:假手术组、缺血再灌注组和低分子肝素组,每组18只. ②应用免疫组化方法测定海马CA1区神经元细胞凋亡基因Bcl-2,Bax表达情况. ③采用两样本均数的t检验对两组间数据进行分析. 结果:大鼠54只均进入结果分析,缺血再灌注组大鼠脑缺血再灌注6,12,24 h时Bcl-2蛋白在神经元内表达的阳性细胞数较低分子肝素组同一时间点明显减少,两组比较具有显著的统计学意义(P＜0.05). 缺血再灌注组大鼠脑缺血再灌注6,12,24 h时Bax蛋白表达的阳性细胞数较低分子肝素组同一时间点明显增加,两组比较具有显著的统计学意义(P＜0.05). 结论:脑缺血再灌注损伤随再灌注时间延长而加重,低分子肝素可能通过减少Bax蛋白的表达,上调Bcl-2蛋白表达,从而减轻神经元的损伤及凋亡,起到脑保护作用.

Effect of low molecular weight heparin on the expressions of Bcl-2, Bax and its neuroprotective effects after focal cerebral ischemia/reperfusion in rats

AIM: To study the effect of low molecular weight heparin on the expressions of Bcl-2, Bax and its neuroprotective effects after focal cerebral ischemia reperfusion in rats. METHODS: Totally 54 male SD rats, with the body mass of 280-330 g were selected and randomly assigned into 3 groups: sham operation group, ischemia/reperfusion group, low molecular weight heparin group with 18 in each group. The expressions of Bcl-2, Bax were checked by immunohistochemistry in hippocampal CA1 subregion. All data in the groups were analyzed with t test. RESULTS: Totally 54 rats were involved in the result analysis. Bcl-2 positive cell number in the ischemia/reperfusion group decreased significantly as compared with that in the low moleucular heparin group at 6, 12, 24 h of reperfusion (P<0.05). Bax expression was significantly decreased in the low molecular weight heparin group, as compared with that in the ischemia/reperfusion group at 6, 12, 24 h of reperfusion (P<0.05). CONCLUSION: Low molecular weight heparin can increase the expression of Bcl-2, decrease the expression of Bax, alleviate the pathological change induced by cerebral ischemia/reperfusion. Low mole-cular weight heparin exerts the neuroprotective effect against the brain injury induced by cerebral ischemia/reperfusion by res-training cell apoptosis.