Protective Effect of Patchouli Alcohol Against SH-SY5Y Cell Injury Induced by Aβ_25-35via the Reduction of Oxidative Stress and Apoptosis

Abstract

Patchouli alcohol (PA) has multiple pharmacological activities, but its protective effect against SH-SY5Y cell injury induced by Aβ25-35 has not been reported. It has been recorded that phosphatidylinositol 3-hydroxykinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway plays an important role in neuroprotection. The purpose of this study was to investigate the protective effect of PA against SH-SY5Y cell injury induced by Aβ25-35 and its underlying mechanism. The results showed that compared with that in the Aβ25-35-induced injury group, the survival rate of SH-SY5Y cells increased ( P < .01) in the different PA-treated groups and the lactic dehydrogenase activity decreased significantly ( P < .01) in the 10, 20, and 40 μg/mL PA groups; compared with those in the Aβ25-35-induced injury group, the malonyldialdehyde contents in SH-SY5Y cells decreased ( P < .05 or P < .01), while the superoxide dismutase, glutathione peroxidase, and catalase activities increased significantly ( P < .05 or P < .01) in the different PA-treated groups; compared with those in the Aβ25-35-induced injury group, the apoptosis rates, and the mRNA and protein levels of Caspase-3 and Bax in SH-SY5Y cells decreased ( P < .05 or P < .01), while the mRNA and protein levels of Bcl-2, and phosphorylated Akt (p-Akt) and phosphorylated mTOR protein levels increased significantly ( P < .05 or P < .01) in the different PA-treated groups. The above results indicate that PA can inhibit the oxidative stress and apoptosis of SH-SY5Y cells induced by Aβ25-35 by regulating the PI3K/Akt/mTOR pathway, to protect the SH-SY5Y cells from the injury induced by Aβ25-35.