SH-SY5Y型
蛋白激酶B
氧化应激
细胞凋亡
超氧化物歧化酶
化学
PI3K/AKT/mTOR通路
谷胱甘肽过氧化物酶
过氧化氢酶
药理学
内分泌学
内科学
生物化学
生物
医学
细胞培养
遗传学
神经母细胞瘤
标识
DOI:10.1177/1934578x211031715
摘要
Patchouli alcohol (PA) has multiple pharmacological activities, but its protective effect against SH-SY5Y cell injury induced by Aβ 25-35 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 Aβ 25-35 and its underlying mechanism. The results showed that compared with that in the Aβ 25-35 -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 Aβ 25-35 -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 Aβ 25-35 -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 Aβ 25-35 by regulating the PI3K/Akt/mTOR pathway, to protect the SH-SY5Y cells from the injury induced by Aβ 25-35 .
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