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.

广藿香醇 (PA) 具有多种药理活性，但其对 Aβ _25-35诱导的 SH-SY5Y 细胞损伤的保护作用尚未见报道。据记载，磷脂酰肌醇 3-羟激酶 (PI3K)/蛋白激酶 B (Akt)/哺乳动物雷帕霉素靶点 (mTOR) 通路在神经保护中起重要作用。本研究的目的是研究 PA 对 Aβ _25-35诱导的 SH-SY5Y 细胞损伤的保护作用及其潜在机制。结果显示，与Aβ _25-35损伤组相比， 不同PA处理组SH-SY5Y细胞存活率增加（P < .01），乳酸脱氢酶活性显着降低（P < .01) 在 10、20 和 40 μg/mL PA 组中；与Aβ _25-35损伤组相比，SH-SY5Y 细胞丙二醛含量降低（P  < .05 或P  < .01），而超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶活性显着升高（P  < .05 或P  < .01) 在不同的 PA 治疗组中；与Aβ _25-35损伤组相比，SH-SY5Y 细胞凋亡率、Caspase-3、Bax mRNA 和蛋白水平降低（P  < .05 或P < .01)，而 不同 PA 治疗组中 Bcl-2 的 mRNA 和蛋白质水平以及磷酸化 Akt (p-Akt) 和磷酸化 mTOR 蛋白水平显着增加（P  < .05 或P < .01）。上述结果表明，PA可以抑制诱导AβSH-SY5Y细胞的氧化应激和细胞凋亡_25-35通过调节PI3K / Akt / mTOR途径，以保护SH-SY5Y细胞免于Aβ引起的损伤_25-35 .