To investigate the effect of musk on AD model rats and its potential mechanism based on Wnt/β-catenin signaling pathway
Objective:To study the neuroprotective effect of musk on Aβ25-35-induced Alzheimer disease(AD)model rats and potential mechanism.Methods:The AD model was established by injecting Aβ25-35 oligomers into the hippocampus of rats,and drug intervention was performed after randomization.Morris water maze was used to evaluate the effects of musk on learning and memory ability of rats.The pathological alterations in rats were detected by H&E staining and Nissl staining techniques.The protein expression and levels of inflammatory factors(IL-1β,IL-6 and TNF-α)were assessed by Western blot(WB),immunohistochemistry and Elisa to investigate the therapeutic effect and potential mechanism of musk on AD model rats.Results:Compared with model group,the escape latency of rats in Musk 200 mg·kg-1 group was shortened with increased residence time in target quadrant and increased number of crossing times in target quadrant.The expressions of GSK-3β(Ser9),PP2A and β-catenin protein in the hippocampus of rats in the musk 200 mg·kg-1 group were significantly increased,and the levels of inflammatory markers(IL-1β,IL-6 and TNF-α)in the cerebral cortex was significantly decreased.Conclusion:Musk may alleviate memory and learning impairment in AD model rats by activating Wnt/β-catenin signaling pathway and reducing inflammation.
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