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目的:观察滋阴活血解毒方对MCAO局灶性脑缺血大鼠脑组织MCP-1、NF-κBp65的表达,探讨其对急性脑缺血后炎症反应的干预作用。方法:将32只SD大鼠随机分为假手术组、模型组、滋阴活血解毒方组(以下简称中药组)和阿加曲班组,每组8只。假手术组仅分离各血管,不做模型处理,其余3组均造MCAO模型,在术后24h断头取脑,采用免疫组化法分析脑缺血部位脑组织MCP-1、NF-κBp65的表达。结果:模型组MCP-1表达高于假手术组(P<0.05),中药组、阿加曲班组MCP-1表达高于假手术组,差异无统计学意义(P>0.05);中药组与阿加曲班组均能降低MCP-1的表达,与模型组比较,差异有统计学意义(P<0.05)。模型组、中药组、阿加曲班组NF-κBp65表达显著高于假手术组(P<0.001),中药组与阿加曲班组均能降低NF-κBp65的表达,与模型组比较,差异有统计学意义(P<0.001)。中药组与阿加曲班组MCP-1、NF-κBp65表达比较无统计学意义(P>0.05)。结论:滋阴活血解毒方能通过抑制炎症因子MCP-1、NF-κBp65的表达,减轻脑缺血后炎症反应。
Objective: To observe the expression of MCP-1 and NF-κB p65 in the brain tissue of MCAO focal cerebral ischemia rats after Ziyin Huoxue Jiedu Decoction, and to explore its intervention effect on inflammatory reaction after acute cerebral ischemia. Methods: Thirty-two SD rats were randomly divided into sham operation group, model group, Ziyin Huoxue Jiedu Fang group (hereinafter referred to as TCM group) and argatroban group, with 8 rats in each group. The sham-operation group only separated the blood vessels and did not model treatment. The other three groups were made MCAO model, at 24 hours after decapitation brain, immunohistochemical analysis of cerebral ischemia brain tissue MCP-1, NF-κBp65 expression. Results: The expression of MCP-1 in model group was higher than that in sham-operation group (P <0.05). MCP-1 expression in Chinese medicine group and argatroban group was higher than that in sham operation group (P> 0.05) Argatroban group could reduce the expression of MCP-1, compared with the model group, the difference was statistically significant (P <0.05). The expression of NF-κBp65 in model group, traditional Chinese medicine group and argatroban group was significantly higher than that in sham-operated group (P <0.001), and both of Chinese medicine group and argatroban group could reduce the expression of NF-κBp65 compared with model group Significance (P <0.001). The expression of MCP-1 and NF-κBp65 in Chinese medicine group and argatroban group had no statistical significance (P> 0.05). Conclusion: Nourishing Yin and Promoting Blood Circulation toxin can relieve the inflammatory reaction after cerebral ischemia by inhibiting the expression of inflammatory factors MCP-1 and NF-κBp65.