摘要
目的:探讨盐酸丁咯地尔对周围神经损害后神经元保护机制。方法:采用SD大鼠,随机分为正常组、模型组、预处理组(盐酸丁咯地尔组),预处理14天后制作坐骨神经损害动物模型,分别在模型制备后6h、12h、24h、48h、72h、96h、7天各组提取L1～5背根神经节作免疫组化计数Bcl-2、Bax阳性细胞表达数,并加以组间比较。结果:(1)预处理组于模型制备后12hBcl-2即有明显表达,24～48h达高峰,持续7天时与模型组比较仍有显著性差异(P<0.05);(2)预处理组Bax蛋白表达与同期模型组均有不同程度降低,7天时表达到最低值,与模型组比较有显著性差异(P<0.05)。结论:盐酸丁咯地尔的神经元保护作用与其上调bcl-2蛋白、抑制Bax蛋白的表达有关。
Objective：To explore protective mechanism of buflomedil Hydrochloride on the neuron of damaged Sciatic nerve in rats. Methods：SD rats were divided into normal, model,buflomedil hydrochloride group in random. Preconditioned for 14 days, the sciatic nerve lesion models were performed, the Bcl-2 and Bax positive cells were counted by immmunohistochemistry at the end of 6h,12h,24h,48h,72h,96h,7days respectively. Results： （1） At the end of 12h after the model perfomed,The expressions of Bcl-2 in buflomedil hydrochloride group increased obvionsly than the normal and model groups,peaked at 24-48h, and at the end of 7days,the expressions of Bcl-2 in buflomedil hydrochloride group increased obviously compared with model group.（2）The expressions of Bax in buflomedil hydrochloride groug were lower than the normal and model groups in the same periods,and that was the lowest at the end of 7 days,It was different significantly than that of model group （P〈0.05）. Conclusion：Buflomedil hydrochloride might upregnlated the expressions of Bcl-2 and downregnlated the expressions of Bax in neuron damaged sciatic nerve,which might be contributed to their protective effects.
出处
《重庆医科大学学报》
CAS
CSCD
2007年第4期359-361,共3页
Journal of Chongqing Medical University
基金
江苏省常州市卫生局资助项目(编号:2004182)。
