RESUMEN
This study was aimed to explore the mechanism ofZi-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 enzymeα (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.
RESUMEN
This study was aimed to observe different forms of β-amyloid peptide (Aβ) and insulin degrading enzyme (IDE) in the hippocampus and cortex in order to further explore the role of Aβ and IDE on spleen yin deficiency di-abetes-associated cognitive decline (DACD), and the effect of Zi-Bu Pi-Y in method. The rats were randomly divided into five groups, which were the blank control (Cont) group, diabetes (DM) group, spleen yin deficiency (pi) group, spleen yin deficiency diabetes (piDM) group and Zi-Bu Pi-Y in recipe (ZBPYR) group. Soluble and insoluble Aβ in the hippocampus and cortex of rats were extracted by gradient centrifugation, and then measured by ELISA. The ex-pression of IDE was observed by western blot. The results showed that the content of soluble and insoluble Aβ1-42 in the hippocampus and cortex of the DM group and piDM group were higher than the Cont group. The soluble and in-soluble Aβ1-42 content in the hippocampus and cortex of the ZBPYR group were reduced compared with the DM group and the piDM group. The soluble Aβ1-40 in the cortex of the DM group, pi group and piDM group were in-creased compared with the Cont group (P < 0.05). The soluble Aβ1-40 content of the ZBPYR group was decreased compared with the DM group and the piDM group (P < 0.05). The expression of IDE protein was decreased in the hippocampus of the DM group and the piDM group compared with the Cont group (P< 0.05), and the IDE protein level in the hippocampus of the ZBPYR group was increased compared with the DM group and the piDM group (P<0.05). The expression of IDE protein in the cortex of the DM group, pi group and piDM group was lower than the Cont group (P< 0.05). The IDE protein level in the cortex of the ZBPYR group was reduced compared to the DM group (P< 0.05). It was concluded that the increased Aβ1-42 in brain may be a major pathological change of DACD and spleen yin deficiency DACD. The decreased IDE expression may be one of the reasons to induce increasing of Aβ1-42 level. The Zi-Bu Pi-Y in method may decrease the Aβ1-42 content by upregulating IDE protein expression.