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Anti-Apoptotic Effects Of Diosgenin In D-Galactose-Induced Aging Brain

Shiu-Min Cheng, Ying-Jui Ho, Shao-Hong Yu, Yi-Fan Liu, Yi-Yuan Lin, Chih-Yang Huang, Hsiu-Chung Ou, Hai-Liang Huang, Shin-Da Lee

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The purpose of this study was to evaluate the effects of diosgenin on the D-galactose-induced cerebral cortical widely dispersed apoptosis. Male 12-week-old Wistar rats were divided into four groups: Control (1[Formula: see text]mg/kg/day of saline, i.p.), DD0 (150[Formula: see text]mg/kg/day of D-galactose, i.p.), DD10, and DD50 (D-galactose[Formula: see text] or 50[Formula: see text]mg/kg/day of diosgenin orally). After eight weeks, histopathological analysis, positive TUNEL and Western blotting assays were performed on the excised cerebral cortex from all four groups. The TUNEL-positive apoptotic cells, the components of Fas pathway (Fas, FADD, active caspase-8 and active caspase-3), and mitochondria pathway (t-Bid, Bax, cytochrome [Formula: see text], active caspase-9 and active caspase-3) were increased in the DD0 group compared with the control group, whereas they were decreased in the DD50 group. The components of survival pathway (p-Bad, Bcl-2, Bcl-xL, IGF-1, p-PI3K and p-AKT) were increased in the DD50 group compared to the control group, whereas the levels of Bcl-xL, p-PI3K, and p-AKT were also compensatorily increased in the DD0 group compared to the control group. Taken together, diosgenin suppressed D-galactose-induced neuronal Fas-dependent and mitochondria-dependent apoptotic pathways and enhanced the Bcl-2 family associated pro-survival and IGF-1-PI3K-AKT survival pathways, which might provide neuroprotective effects of diosgenin for prevention of the D-galactose-induced aging brain.