滋补肝肾复方对MCAO大鼠脑组织MLCP的调控作用

Regulating effect of compound prescription of nourishing liver and kidney on cerebral expression of MLCP in rats with MCAO

关键词:  滋补肝肾复方  脑梗死  神经再生  抑制因子  MLCP

Key words:  compound prescription of nourishing liver and kidney  cerebral infarction  neural regeneration  inhibiting factor  MLCP

摘要:

[目的] 观察滋补肝肾复方对脑梗死大鼠神经功能、脑梗死体积及脑组织肌球蛋白轻链磷酸酶(MLCP)的影响,探讨其解除神经再生抑制的机制。[方法] 60只SD大鼠随机分为正常对照组、假手术组、模型组和药物组共4个组。用改良的Longa EZ法制备大脑中动脉阻塞大鼠模型,药物组灌胃给予滋补肝肾复方水溶液,余各组分别灌胃给予同剂量的蒸馏水。观察了治疗后各组大鼠的神经功能和脑组织梗死体积,用免疫组织化学法观察模型大鼠梗死周边区脑组织MLCP的表达。[结果] 药物组与模型组比较显示,药物组大鼠的神经功能明显优于模型组,且梗死体积较模型组明显缩小,免疫组化研究显示药物组脑组织中MLCP表达虽然较正常对照组增多,但较模型组明显减少,两者之间有差异有统计学意义(P<0.05).[结论] 滋补肝肾复方可改善神经功能,缩小脑梗死体积,抑制MLCP在脑梗死后的表达,从而促进神经发生。

Abstract:

[Objective] To explore the mechanism of compound prescription of nourishing liver and kidney (NLKC) promoting neural regeneration by observing the effect of neural function deficient scale, brain infarct volume, NLKC on the expression of MLCP in rats with cerebral infarction. [Methods] The 60 SD rats were randomly divided into normal control, sham operation, model and medicine groups. The rat models with middle cerebral artery occlusion were successfully established by the improved Longa EZ. The neural function deficient scale and brain infarct volume were investigated after the treatment. The treated groups were given with NLKC. Other group were given with commensurability distilled water. The expressions of MLCP in the region around the infarction were observed by immunohistochemical method. [Results] It was great significant to neural function and brain infarct volume between medicine group and model group(P<0.01). The difference of MLCP expression between medicine group and model group was significant(P<0.05). [Conclusion] The NLKC can promote neurogenesis by inhibiting the expression of MLCP, improve the neural function and reduce the brain infarct volume.