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目的研究利开灵对脑出血后脑水肿的保护作用及可能的作用机制,进而探讨开通玄府、利水解毒法在脑出血后脑水肿中的作用。方法采用Rosenberg法改良后建立胶原酶诱导大鼠脑出血模型(n=9),造模后每隔12 h给予利开灵浓煎剂灌胃,于12、24、48、72 h每组3只灌注固定后取大鼠脑组织做常规HE染色,观察各组大鼠病理变化;每组6只对新鲜脑组织取材,W esternblotting方法检测脑组织水通道蛋白-4(AQP4)含量。结果在病理形态学方面,各时间点模型组大鼠较假手术组大鼠血肿区可见大量红细胞浸润,神经细胞坏死,无正常脑组织结构。利开灵组大鼠病理改变明显轻于各时间点的模型组大鼠。脑出血12、24、48、72 h模型组较相应时间点假手术组脑组织AQP4蛋白表达升高(P<0.05,P<0.01),除脑缺血12 h利开灵组外,其他时间点利开灵组较相应时间点模型组脑组织AQP4蛋白表达降低(P<0.05,P<0.01),初步得到脑出血12 h到72 h模型组脑组织AQP4蛋白表达的曲线,在12 h脑组织AQP4蛋白表达较低,在24 h表达较高持续到72 h,72 h模型组脑组织AQP4蛋白较12 h模型组升高(P<0.05)。结论利开灵通过对脑组织AQP4蛋白表达的调节,减轻脑出血后神经细胞肿胀,减轻脑水肿,有效保护脑组织。
Objective To study the protective effects of likailing on cerebral edema after intracerebral hemorrhage and its possible mechanism, and then to explore the role of Kai-sheng and Li-shui detoxification in cerebral edema after intracerebral hemorrhage. Methods Rosenberg method was used to establish collagenase-induced intracerebral hemorrhage model (n = 9). The model rats were given intragastric administration of RKL once every 12 hours. At 12, 24, 48 and 72 h, After perfusion and fixation, the brain tissues of rats were sacrificed and their histopathological changes were observed by HE staining. Six rabbits in each group were drawn from fresh brain tissue and the content of aquaporin-4 (AQP4) in brain tissue was detected by Western blotting. Results In pathomorphology, there were a large number of erythrocyte infiltration, necrosis of nerve cells and no normal brain tissue in the hematoma of rats in model group at each time point. The pathological changes in the Kailingling group were lighter than those in the untreated group at each time point. At 12, 24, 48 and 72 h after cerebral hemorrhage, the expression of AQP4 protein increased (P <0.05, P <0.01) in sham operation group at 12, 24, 48 and 72 h, The expression of AQP4 protein in the model group at each time point was significantly lower than that in the model group at the corresponding time point (P <0.05, P <0.01), and the curve of AQP4 protein expression in the model group at 12 h to 72 h after cerebral hemorrhage was obtained. Tissue AQP4 protein expression was low at 24 h expression was sustained up to 72 h, 72 h model group brain tissue AQP4 protein increased compared with the 12 h model group (P <0.05). Conclusion LiKailing can regulate the expression of AQP4 protein in brain tissues, relieve the swelling of neurons after cerebral hemorrhage, relieve brain edema and effectively protect the brain tissue.