Oxidative stress is a major component of harmful cascades activated in
neurodegenerative disorders. Here, we tried to elucidate the possible
neuroprotective effect of
Salvigenin, a natural polyphenolic compound, on oxidative stress-induced apoptosis and autophagy in human
neuroblastoma SH-SY5Y cells. We measured cell viability by MTT test and found that 25 μM is the best protective concentration of
Salvigenin. GSH and SOD assays suggested that
Salvigenin activates
antioxidant factors. At the same time, measurement of ER stress-associated
proteins including
calpain and
caspase-12 showed the ability of
Salvigenin to decrease ER stress. We found that
Salvigenin could decrease the apoptotic factors.
Salvigenin inhibited H(2)O(2)-induced
caspase-3 which is a hallmark of apoptosis in addition to reducing Bax\Bcl-2 ratio by 1.45 fold. Additionally,
Salvigenin increased the levels of autophagic factors. Our results showed an increase in LC3-II/LC3-I ratio, Atg7, and Atg12 in the presence of 25 μM of
Salvigenin by about 1.28, 1.25, and 1.54 folds, respectively, compared to H(2)O(2)-treated cells. So it seems that H(2)O(2) cytotoxicity mainly results from apoptosis. Besides,
Salvigenin helps cells to survive by inhibiting apoptosis and enhancing autophagy that opens a new horizon for the future experiments.