RESUMO
This study was aimed to observe the protection ofZi-Bu Pi-Yin recipe (ZBPYR) on the cortex mitochondrial dysfunction of diabetes-associated cognitive dysfunction rats. SD rats were randomly divided into four groups, which were the control (Con) group, the diabetes (DM) group, the ZBPYR treatment (ZBPYR1) group and the ZBPYR protection (ZBPYR2) group. Morris water maze test was taken to evaluate the learning and memory ability of rats. The transmission electron microscope (TEM) was used to detect the ultrastructure and quantity changes of cortex mitochondria. Western blot was used to detect the expression of Cyto C. The results showed that compared to Con group, the learning and memory ability were decreased in the DM group (P < 0.05); the learning and memory ability of the ZBPYR1 group was improved compared to the DM group (P < 0.05); compared to the DM group, the ZBPYR2 group was significantly improved (P < 0.01). Compared with the Con group, the number of cortex mitochondria in DM group was decreased (P< 0.05), and the structure was disordered, blurred, or even completely destroyed. After ZBPYR intervention, these pathological changes were reduced obviously. And the number of mitochondria in the ZBPYR2 group was increased than that of the DM group (P < 0.05). The expression of Cyto C in cytoplasm of the DM group was significantly higher than that of the Con group (P < 0.01). After ZBPYR intervention, the expression of Cyto C was decreased. It was concluded that ZBPYR regulated the mitochondrial morphology and changes of volume in the cortex, prevented the releasing of Cyto C from mitochondria to cytoplasm, and improved the cognitive function of diabetes rats.
RESUMO
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.
RESUMO
This study was aimed to observe the effect ofZi-Bu Pi-Yin Recipe (ZBPYR) on the mRNA expressions of NMDA receptor subunits NR1, NR2A, NR2B in different brain regions of spleen-yin deficiency Alzheimer's Disease (AD) model rats. The levels of NR1, NR2A, NR2B mRNA expressions were detected by using RT-PCR method. The results showed that the levels of NR1, NR2A, NR2B mRNA expressions of AD group and spleen-yin deficiency AD group decreased significantly (P < 0.05). The levels of NR1, NR2A, NR2B mRNA expressions of ZBPYR treatment group increased significantly (P < 0.05). It was concluded that the expression levels of NMDAR mRNA in different brain regions of the ZBPYR treatment group increased significantly, which indicated that ZBPYR may up-regulate the protein expressions of NMDAR by increasing the expression levels of NMDAR mRNA, thereby to play the anti-dementia effect.