Empirical Study of Proteome of Hippocampus from A Rat Model with Alzheimer's Disease with Spleen Deficiency Syndrome Effected by Zibu Piyin Recipe

The article is aimed at investigating Alzheimer's disease (AD) with spleen yin deficiency syndrome and identifying the effective therapeutic targets of Zibu Piyin Recipe (ZBPYR) at whole cell protein levels. The rat model of spleen yin deficiency syndrome was set up through combination with improper diet, overstrain, and consumption of body fluid. Then, the polymerized β-amyloid 1–40 was injected into both hippocampi of the rats. The treated group was administered with ZBPYR. Taking the control group as a standard, the changes of proteins in the hippocampus were compared between the model group of AD with spleen yin deficiency syndrome and ZBPYR-treated group by two-dimensional gel electrophoresis. The altered protein spots were analyzed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS). Compared with the control group, 9 protein spots of the hippocampus in the model group of AD with spleen yin deficiency syndrome and 2 spots in ZBPYR-treated group were found to be changed totally. The differential protein spots were identified by MALDI-TOF-MS. The results showed that in the model group of AD with spleen yin deficiency syndrome, the level of annexin III was higher, but the levels of tubulin beta chain 15, dihydropyrimidinase-like 2, and guanine nucleotide-binding protein beta-1 subunit were lower than that of the control group. These differential proteins did not show significant changes between the ZBPYR-treated group and the control group. It is concluded that changes of several proteins in the hippocampus may involve in the pathogenesis of AD with spleen yin deficiency syndrome together. Annexin III, tubulin beta chain 15, dihydropyrimidinase-like 2, and guanine nucleotide-binding protein beta-1 subunit are possibly related to pathological changes of the hippocampus in AD with spleen yin deficiency syndrome. ZBPYR may produce its effects by regulating these proteins in the hippocampus.