Journal
MOLECULAR AND CELLULAR BIOCHEMISTRY
Volume 371, Issue 1-2, Pages 9-22Publisher
SPRINGER
DOI: 10.1007/s11010-012-1416-6
Keywords
Apoptosis; Autophagy; Oxidative stress; Salvigenin; SH-SY5Y neuroblastoma cells
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Funding
- Shahid Beheshti University of Medical Sciences Research Funds
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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 mu M 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 H2O2-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 mu M of Salvigenin by about 1.28, 1.25, and 1.54 folds, respectively, compared to H2O2-treated cells. So it seems that H2O2 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.
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