头针对急性脑缺血再灌注大鼠脑内Bax、Fas、caspase-3的影响

目的：观察头针对脑缺血再灌注后大鼠脑神经元损伤的保护作用,探讨头针治疗脑缺血的可能机制。方法：90只健康SD雌性大鼠随机分为假手术组10只,模型组和头针组各40只。采用大脑中动脉线栓法将模型组和头针组大鼠制备大脑中动脉闭塞（MCAO）再灌注模型,头针组大鼠给予头针治疗。观察治疗6、24、48及72h各时相点各组大鼠神经功能缺损（NSS）评分,脑组织Bax、Fas及caspase-3的表达。结果：①NSS评分：造模后各时相上点组间比较,头针组与模型组NSS评分显著高于假手术组（P〈0.01）;在第72h时相点头针组NSS评分显著低于模型组（P〈0.01）。②Western bloting检测：造模后6、24、48和72h时相点头针组及模型组Bax蛋白在梗死侧脑组织中均有表达,且在24h达高峰,随着时间推移,模型组的Bax蛋白相对光密度比值较头针组减少缓慢（P〈0.01）。③RT-PCR检测：头针组与模型组Fas、caspase-3mRNA在梗死边缘区的内侧诱导表达,头针组明显少于模型组。结论：脑缺血损伤诱导Bax、caspase-3、Fas基因表达增强,Bax、caspase-3、Fas在介导神经细胞凋亡和缺血性脑损害中起关键作用。使用头针治疗对脑缺血再灌注后大鼠脑组织有保护作用。

The Effects Of Scalp-acupuncture on Bax, Fas, and Caspase-3 in Brain of Rats with Acute Cerebral Ischemia Reperfusion Injury

Objective.. To explore the protective effects of scalp-acupuncture （SA） on brain neuron injury following cerebral ischemia/repeffusion in rats and the possible mechanisms of SA in treating brain ischemia. Methods.. Ninety healthy SD female rats were randomly divided into sham-operated group （n=10）, model group （n=40）, and SA treatment group （n=40）. Rat models of middle cerebral artery （MCA） ischem-reperfusion were prepared by middle cerebral artery occlusion （MCAO） in model and SA treatment group. The changes of neurofunctional defect, and the expression of Bax, Fas and caspase-3 were observed at 6th, 24th, 48th, and 72nd h after treatments. Results： （1） The NSS scores in model and SA treatment groups were significantly higher than in shamoperated group （P≤0.01） at each time point. At 72nd h, the NSS scores in SA group were markedly lower than in model group （P〈0.01）. （2） At 6th, 24th, 48th, and 72nd h after modeling, the expression of Bax protein was detectable in both SA and model groups, and reached the peak at 24th h. With time over, the expression level of Bax protein in model group was reduced slowly as compared with SA group. （3） The expression of caspase-3 and Fas mRNA was detected in the margin of the infarction area, and the expression levels of caspase-3 and Fas mRNA in SA group were significantly higher than in model group. Conclusion：Cerebral ischemia induced the enhanced expression of Bax, caspase-3, and Fas mRNA. Bax, caspase-3, and Fas play important roles in mediating neurons apoptosis and isehemic brain injury. SA can protect the brain from ischemia-reperfusion injury in rats.