Cornin protects SH-SY5Y cells against oxygen and glucose deprivation-induced autophagy through the PI3K/Akt/mTOR pathway

It has been reported that cornin may reduce neuronal death during cerebral ischemia; however, little is known about the molecular mechanism of the role of corninin autophagy in SH-SY5Y neuronal cells. In the present study, oxygen-glucose deprivation (OGD)-treated cells were used as a cerebral ischemia model in vitro. The results demonstrated that cornin was able to reduce neuronal cell loss, increase the apoptosis regulator Bcl-2/apoptosis regulator BAX ratio, and decrease the protein levels of caspase-3. In addition, cornin decreased the microtubule-associated proteins 1A/1B light chain 3B (LC3)-II/LC3-I ratio and beclin-1 protein expression, and resulted in an upregulation in phosphorylated (p)-RAC- serine/threonine-protein kinase (Akt), p-protein kinase mTOR (mTOR) in OGD-treated SH-SY5Y cells. Additionally, it was observed that following inhibition of PI3K/Akt by LY294002, the levels of p-Akt and p-mTOR were markedly decreased, and the LC3-II/LC3-I ratio and beclin-1 were increased. Similarly, following inhibition of mTOR by rapamycin, LC3-II/LC3-I and Beclin-1 were significantly increased in SH-SY5Y cells. These results indicated that cornin protected SH-SY5Y cells against OGD-induced autophagy through the PI3K/Akt/mTOR pathway.