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目的:探究姜黄素对脑缺血大鼠脑组织PI3K/Akt信号转导通路的影响及作用机制。方法:将72只SD大鼠随机分为假手术组、模型组、姜黄素A组和姜黄素B组,每组18只。其中模型组、姜黄素A、B组慢性脑缺血大鼠模型制备采用将大鼠两侧颈动脉结扎的方法,假手术组和模型组大鼠分别给予等剂量生理盐水。采用免疫组化法检测大鼠PI3K、AKT、Bcl-2、BAX蛋白表达情况,采用干湿重法检测脑组织水含量,采用甲酰胺法检测血脑屏障通透性。结果:与模型组比较,姜黄素组大鼠PI3K、AKT、Bcl-2蛋白含量均明显增高(P<0.05,P<0.01,P<0.05),脑组织含水量、BAX表达及伊文思蓝含量显著降低(P<0.05,P<0.01,P<0.01),差异均具有统计学意义。结论:姜黄素对缺血性脑损伤的保护机制可能是其穿透血脑屏障后激活了PI3K/AKT信号通路,介导Bcl-2蛋白表达增加以及BAX蛋白表达降低,进而调节二者平衡。
Objective: To investigate the effect of curcumin on PI3K / Akt signal transduction pathway in brain tissue of ischemic rats and its mechanism. Methods: Seventy-two SD rats were randomly divided into sham-operation group, model group, curcumin group A and curcumin group B, with 18 rats in each group. The model group, curcumin A, B group were prepared by chronic carotid artery occlusion on both sides of the carotid artery in rats, sham operation group and model group rats were given equal doses of saline. The expression of PI3K, AKT, Bcl-2 and BAX proteins were detected by immunohistochemistry. The water content of brain tissue was determined by wet and dry method. The permeability of blood-brain barrier was detected by formamide method. RESULTS: Compared with the model group, the protein levels of PI3K, AKT and Bcl-2 in curcumin group were significantly increased (P <0.05, P <0.01, P <0.05), the content of brain water, BAX expression and Evans blue content (P <0.05, P <0.01, P <0.01), the differences were statistically significant. CONCLUSION: The protective mechanism of curcumin on ischemic brain injury may be that PI3K / AKT signaling pathway is activated after it penetrates the blood-brain barrier, which mediates the increase of Bcl-2 protein expression and the decrease of BAX protein expression, thereby regulating the balance between them.