复健片对不同时相脑梗死大鼠脑组织微管相关蛋白-2表达的影响

Effect of Fujian Tablets on Expression of Microtubule-associated Protein 2 in Cerebral Infarction Rats at Different Time Points

【目的】观察滋补肝肾中药复健片在不同时相对脑梗死大鼠脑组织微管相关蛋白-2(MAP-2)表达的影响,探讨其促进神经干细胞分化的作用机制及MAP-2在脑梗死后的动态变化。【方法】选用240只SD大鼠随机分为正常对照组、假手术组、模型组和中药组,并根据脑梗死病程每组又分为3、7、14、28、42 d共5个亚组,每个亚组动物数为12只。采用改良的Longa法行大脑中动脉阻塞复制大鼠局灶性脑缺血模型,中药组灌胃给予复健片水溶液(剂量为9 g·kg-1.d-1),其他各组分别灌胃给予同剂量的蒸馏水。【结果】模型组大鼠脑梗死后3 d时,脑组织MAP-2表达即达到高峰,与正常对照组比较差异有显著性意义(P<0.0001),后逐渐下降,至第14天时降至正常水平,与正常对照组比较差异无显著性意义(P>0.05)。中药组在3 d时MAP-2出现高表达,7 d时其表达达到高峰,持续至14 d时开始下降。不同时相中药组的MAP-2表达与模型组比较差异均有显著性意义(P<0.01或P<0.0001)。【结论】复健片促进中枢神经再生作用与其能增加脑梗死后脑组织MAP-2的表达有关。

Objective To observe the effect of Fujian Tablets （FT）, a prescription with the actions of nourishing liver and kidney, on the expression of microtubule-associated protein 2 （ MAP-2 ） in cerebral infarction rats at different time points, and to explore its mechanism on promoting nerve cell differentiation. Methods A total of 240 male Sprague Dawley rats were divided into normal control group, sham-operation group, model group and FT group. Focal cerebral ischemia models were established by occlusion of the middle cerebral artery according to the reformed Longa method in rats, and were subdivided into 3-, 7-, 14-, 28-, and 42-day cerebral infarction subgroups. FT group was given FT in the dose of 9 g·kg^-1·d^-1, and the other groups were given the same dose of distilled water. Results In the model group, MAP-2 expression in the hippocampus increased and reached a peak on day 3, which were notably different from that in the normal control group （ P 〈 0. 0001 ）, and gradually decreased from then on, reduced to normal level on day 14. The difference of MAP-2 expression between the model group and the normal control group was insignificant from day 14 （ P 〉 0.05 ）. In FT group, MAP-2 expression increased on day 3, reached a peak on day 7, remained high level till day 14, and then decreased, the difference being significant compared with the model group （P 〈 0. 01 or P 〈 0. 0001 ）. Conclusion The mechanism of FT on promoting neural regeneration is probably related with the increase of cerebral MAP-2 expression after cerebral infarction.