目的：探讨滋补脾阴方药（ZBPYR）调节自噬及内质网应激（ERS）改善脾阴虚糖尿病认知功能障碍的作用机制。方法：将大鼠随机分为空白对照组（cont），糖尿病组（DM），脾阴虚组（pi），脾阴虚糖尿病组（piDM），脾阴虚糖尿病+滋补脾阴方药治疗组（ZBPYR）。Western Blot观察微管相关蛋白1A/1B轻链3Ⅱ（LC3Ⅱ）、抑制物阻抗性酯酶1α亚基（IRE1α）、c-Jun氨基端激酶（JNK）的蛋白表达。结果：DM组、pi组、piDM组LC3Ⅱ较cont组降低（P<0.05），ZBPYR组LC3Ⅱ较DM组、piDM组增加（P<0.05）。与cont组比较，DM组、piDM组p-IRE1α、pi组、piDM组p-JNK1均有所增加（P<0.05），ZBPYR组p-IRE1α、p-JNK1与DM组、piDM组比较有所降低（P<0.05）。结论：ZBPYR调节自噬及ERS改善脾阴虚糖尿病认知功能障碍。

This study was aimed to explore the mechanism of Zi-Bu Pi-Yin Recipe (ZBPYR) on autophagy and endoplasmic reticulum stress (ERS) to improve spleen-yin deficiency diabetes-associated cognitive decline (DACD). Rats were randomly divided into the control (cont) group, the diabetes (DM) group, the spleen-yin deficiency (pi) group, the spleen-yin deficiency diabetes (piDM) group, and the spleen-yin deficiency diabetes + ZBPYR treatment (ZBPYR) group. The expression of microtubule-associated protein 1A/1B-light chain 3 (LC3Ⅱ), inositol-requiring enzyme α (IRE1α), c-Jun N-terminal kinase (JNK) were observed by western blot. The results showed that the expression of LC3Ⅱ in the DM group, pi group and piDM group decreased compared with the cont group (P < 0.05); and the expression of LC3Ⅱ of the ZBPYR group increased compared with the DM group and piDM group (P < 0.05). Compared with the cont group, the p-IRE1α of the DM group and piDM group, as well as p-JNK1 in the pi group and piDM group were increased (P < 0.05). The p-IRE1α and p-JNK1 of the ZBPYR group were decreased compared with the DM group and piDM group (P < 0.05). It was concluded that ZBPYR improved spleen-yin deficiency DACD by regulating autophagy and ERS.

教育部高等学校博士学科点专项科研基金（优先发展领域）（20132105130001）：蛋白质组学联合计算化学研究滋补脾阴方药改善糖尿病认知功能障碍的多成分多靶点调控机制，负责人：战丽彬；教育部高等学校博士学科点专项科研基金（20112105110006）：滋补脾阴法对糖尿病认知功能障碍的作用及其线粒体相关机制，负责人：战丽彬。