【摘要】 目的 ：探究γ-亚麻酸（GLA）对血管性认知障碍（VCI）的作用及机制。方法 ：将30只雄性C57BL6J小鼠平均分为对照组、VCI组以及GLA组，对VCI组和GLA组行双侧颈动脉结扎建立VCI小鼠模型，对照组进行假手术。VCI组和假手术组每日以1 mg/kg生理盐水灌胃，GLA组每日以1 mg/kg GLA灌胃。14 d后，以Morris水迷宫检测小鼠认知障碍水平，H-E染色观察小鼠脑组织情况，以透射电镜观察海马体组织神经元情况，以免疫印迹检测小鼠PI3K/AKT/mTOR通路相关蛋白、细胞自噬相关蛋白以及神经元凋亡相关蛋白表达水平。结果 ：VCI组小鼠的逃逸潜伏期较GLA组和对照组长，穿越平台次数和目标象限停留时间短于其余2组；GLA组脑组织神经元形态优于VCI组，但较对照组差；VCI组PI3K/AKT/mTOR通路相关蛋白、细胞自噬相关蛋白以及神经元凋亡相关蛋白表达水平高于对照组和GLA组，GLA组高于对照组。结论 ：GLA可通过抑制PI3K/AKT/mTOR通路介导自噬以降低神经元凋亡，以对VCI进行治疗。更多还原

【Abstract】 Objective : To explore the effect and mechanism of gamma-linolenic acid(GLA) on vascular cognitive impairment(VCI). Methods : Thirty male C57BL6J mice were evenly divided into control group, VCI group, and GLA group. The VCI mouse model was established by bilateral carotid artery ligation in the VCI group and GLA group, and the sham operation was performed in the control group. The VCI group and sham group were given 1 mg/kg normal saline daily, while the GLA group was given 1 mg/kg GLA daily. 14 days later, the Morris water maze was used to detect the level of cognitive impairment of mice. The mice were sacrificed and the brain tissue of mice was observed by H-E staining. The neurons in the hippocampus of mice were observed by transmission electron microscopy. Western blotting was used to detect the expression levels of PI3K/AKT/mTOR pathway-related proteins, autophagy-related proteins, and neuronal apoptosis-related proteins in mice. Results :The escape latency of mice in the VCI group was longer than that in the GLA group and control group, and the number of platform crossings and the residence time in the target quadrant were shorter than those in the other two groups. The morphology of neurons in the GLA group was better than that in the VCI group, but worse than that in the control group. The expression levels of PI3K/AKT/mTOR pathway-related proteins, autophagy-related proteins, and neuronal apoptosis-related proteins in the VCI group were higher than those in the control group and GLA group, with the GLA group showing higher levels than the control group. Conclusion : GLA mitigates neuronal apoptosis in treating VCI by suppressing autophagy via the PI3K/AKT/mTOR pathway.更多还原