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目的探讨脑健胶囊对局灶性脑缺血大鼠趋化因子单核细胞趋化蛋白-1(MCP-1)和巨噬细胞炎性蛋白-1α(MIP-1α)的影响。方法将100只大鼠随机分为假手术组、模型组、补阳还五汤组和脑健胶囊组,每组25只,采用大脑中动脉栓塞法建立永久性局灶性脑缺血模型,于术后1d、3d、7d、14d、28d处死,采用ELISA法检测血清中MCP-1、MIP-1α含量,免疫组化法检测脑组织中MCP-1、MIP-1α的阳性表达。结果模型组大鼠自术后1d始血清中MCP-1、MIP-1α含量即较假手术组明显升高(P<0.05或P<0.01),脑健胶囊组大鼠血清中上述指标在各时间点均较模型组降低(P<0.05或P<0.01),且其1d的MCP-1和14d的MIP-1α水平改善均优于补阳还五汤组(P<0.05);模型组脑组织中MCP-1、MIP-1α的阳性表达在术后1d、3d、7d、14d、28d均高于假手术组(P<0.05或P<0.01),脑健胶囊组MCP-1的阳性表达在上述各时间点均较模型组降低(P<0.05或P<0.01),而其MIP-1α的阳性表达从术后7d、开始降低(P<0.05或P<0.01),且脑健胶囊组MIP-1α的阳性表达在术后7d、28d均明显低于补阳还五汤组(P<0.05)。结论脑健胶囊抗脑缺血损伤的保护作用可能与降低MCP-1、MIP-1α水平,进而抑制脑缺血后炎症反应有关。
Objective To investigate the effects of Naokang capsule on the expression of chemokines MCP-1 and MIP-1α in focal cerebral ischemia rats. Methods 100 rats were randomly divided into sham operation group, model group, Buyang Huanwu Decoction group and Naojian Capsule group, with 25 rats in each group. Permanent middle cerebral artery occlusion (MCAO) The rats were sacrificed at 1 day, 3 days, 7 days, 14 days and 28 days after operation. The contents of MCP-1 and MIP-1α in serum were detected by ELISA. The expressions of MCP-1 and MIP-1α in brain tissue were detected by immunohistochemistry. Results The serum levels of MCP-1 and MIP-1α in the model group were significantly higher than those in the sham-operated group (P <0.05 or P <0.01) (P <0.05 or P <0.01), and the levels of MIP-1α in MCP-1 and 14d at 1d were all better than those in Buyanghuanwu Decoction (P <0.05) The positive expression of MCP-1 and MIP-1αin the brain tissues were significantly higher than those in the sham operation group on the 1st, 3rd, 7th, 14th and 28th day postoperatively (P <0.05 or P <0.01) (P <0.05 or P <0.01) at each time point, while the expression of MIP-1α decreased from the 7th day after operation (P <0.05 or P <0.01) The positive expression of MIP-1α was significantly lower than that of Buyanghuanwu Decoction 7d and 28d after operation (P <0.05). Conclusion Naokao Capsule can protect against cerebral ischemia injury by decreasing the levels of MCP-1 and MIP-1α and then inhibiting the inflammatory response after cerebral ischemia.