Classic Famous Prescription Kai-Xin-San Ameliorates Alzheimer ’s Disease via the Wnt/β-Catenin Signaling Pathway

In this study, the AD model rats were established by combining intraperitoneal injection of D-galactose (150 mg/kg/day) and intracerebral injection of Aβ25-35 (10 μL) to investigate the meliorative effect of KXS on AD and explore its mechanism. After 1-month KXS treatment, Morris water maze test showed that different doses of KXS all improved the cognitive impairment of AD rats. The results of hematoxylin and eosin staining, Nissl staining, and Tunnel staini ng showed that the neuron injury in the hippocampal CA1 region of the AD rats was markedly improved after KXS treatment. Concurrently, KXS reversed the levels of biochemical indexes of AD rats. Furthermore, the protein expressions of Wnt1 and β-catenin in KXS groups were remarkably increased, while the expressions of Bax and caspase-3 were significantly decreased. Besides, KXS-medicated serum reduced the levels of tumor necrosis factor-α, interleukin-1β, and reactive oxygen species and regulated the protein expressions of β-catenin, glycogen synthase kinase-3β (GSK-3β), p-GSK-3β, Bax, a nd caspase-3 in Aβ25-35-induced pheochromocytoma cells. Most importantly, this effect was attenuated by the Wnt inhibitor IWR-1. Our results suggest that KXS improves cognitive and memory function of AD rats, and its neuroprotective mechanism may be mediated through the Wnt/ β-catenin signaling pathway.
Source: Molecular Neurobiology - Category: Neurology Source Type: research