NDLI: Increase of autophagy and attenuation of apoptosis by Salvigenin promote survival of SH-SY5Y cells following treatment with H$_{2}$O$

Content Provider	Springer Nature Link
Author	Rafatian, Ghazaleh Khodagholi, Fariba Farimani, Mahdi Moridi Abraki, Shahnaz Babaei Gardaneh, Mossa
Copyright Year	2012
Abstract	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.
Starting Page	9
Ending Page	22
Page Count	14
File Format	PDF
ISSN	03008177
Journal	Molecular and Cellular Biochemistry
Volume Number	371
Issue Number	1-2
e-ISSN	15734919
Language	English
Publisher	Springer US
Publisher Date	2012-08-17
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Apoptosis Autophagy Oxidative stress Salvigenin SH-SY5Y neuroblastoma cells Medical Biochemistry Cardiology Oncology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Clinical Biochemistry Molecular Biology

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