目的 研究中药治疗AD相关机制,探究以益气活血法为组方原则的天芪益智颗粒对AD大鼠脑组织炎性反应的保护作用.方法 90只雄性SD大鼠随机分成6组,每组15只,模型组和治疗组予Aβ1-42在大鼠侧脑室注射建立AD动物模型,造模成功后,治疗组分别灌服浓度为高、中、低剂量的天芪益智颗粒每天一次,对照组灌服石杉碱甲每天一次,空白组和模型组予等量生理盐水每天一次,给药体积均为20 mL/kg体重,分别连续给药30天.喂养30天以后取大鼠脑组织进行蛋白提取,用western blot方法观察各组大鼠脑组织相关蛋白的表达.结果 (1)模型组较空白组GFAP和Iba-1的表达显著增高(P<0.05);(2)天芪益智颗粒和石杉碱甲可使大鼠脑组织GFAP和Iba-1的表达量显著降低(P<0.05);(3)天芪益智颗粒和石杉碱甲使phospho-p38/t-p38的表达量明显降低(P<0.05);(4)天芪益智颗粒使AD大鼠脑iNOS、COX-2表达量显著降低(P<0.05).结论 (1)Aβ1-42侧脑室注射可以模拟AD炎性反应机制;(2)天芪益智颗粒通过抑制脑组织胶质细胞的激活、降低phospho-p38/t-p38表达及p38-NF-κB信号通路激活、抑制促炎因子COX-2、iNOS的表达对AD大鼠炎性反应具有保护作用.%Objective To reveal the related mechanism of Chinese traditional medicine in treatment on AD, and to explore the Yiqihuoxue prescription principle for Tianqi Yizhi granules on the protective effect of inflammatory reaction in brain tissue of AD rats.Methods 90 rats were randomly divided into six groups(15 in each group).Five of them were injected with Aβ1-42 in lateral ventricle to establish AD model rats.Treatment groups were received different doses of Tianqi Yizhi granules, and control group was given huperzine.30 days later the rats were sacrificed and the proteins in brain tissue were extracted, the western blot was applied for determination of protein expression in brain tissue, and the possible mechanism of tradition Chinese medicine in treatment of AD rats was discussed.Results (1) Compared with blank group, the expression levels of GFAP and Iba-1 in model group had significantly increased (P<0.05).(2) The expression of GFAP and Iba-1 had respectively decreased (P<0.05).(3) Tianqi Yizhi granules and huperzine could significantly decreased the expression of phospho-p38/t-p38 (P<0.05).(4) Tianqi Yizhi granules could significantly decreased the expression of iNOS and COX-2 in brain tissue (P<0.05).Conclusion (1)Aβ1-42 lateral ventricle injection could imitate the AD inflammatory reaction mechanism;(2) Tianqi Yizhi Granules play a protective role on the inflammatory reaction in the brain of AD rats by suppressing the activation of glial cells in brain tissues, decreased the expression of phospho-p38/t-p38 and inhibited p38-NF-kappa B signaling pathway activation.Moreover, it can inhibit the expression of COX-2 and iNOS.
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