Anthocyanin ameliorates hypoxia and ischemia induced inflammation and apoptosis by increasing autophagic flux in SH-SY5Y cells.

Inhibition of the oxidative stress induced by hypoxia and ischemia would be beneficial for reducing neuroinflammation and promoting nerve cell survival. We had previously reported a kind of anthocyanin (pentunidin-3-O-rutinoside (p-coumaroyl)-5-O-glucoside) to reduce the damage to neurovascular unit in middle cerebral artery occlusion (MCAO) rats. However, the neuroprotective mechanism of anthocyanin remains to be elucidated. Neuronal autophagy, after ischemic hypoxia, seems to be part of the pro-survival signal. In the current study, we used oxygen and glucose deprivation (OGD) to stimulate SH-SY5Y cells, and observed whether anthocyanin could reduce the inflammatory response and apoptosis, and explored the role of autophagy in this process. Anthocyanin significantly increased the autophagic flux, inhibited oxidative stress, and reduced inflammatory response and neuronal apoptosis in OGD exposed SH-SY5Y cells. The autophagy agonist rapamycin enhanced the anti-inflammatory effect of anthocyanin, while the autophagy inhibitor 3-methyladenine (3-MA) forbade its protective effect. Our finding, therefore, suggested the reduction of hypoxia and ischemia induced oxidative stress, along with inflammation and apoptosis, by anthocyanin, to occur via increase of autophagic flux in SH-SY5Y cells.
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