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Arulkumar k Arul*
The present research was designed to explore the neuroprotective effect of NPIASA against rotenone-induced mitochondrial dysfunction, oxidative stress and apoptosis in a SH-SY5Y human neuroblastoma cellular model. The cells were divided into four experimental groups (control, rotenone (100 nM), NPIASA (5) + rotenone (100 nM), NPIASA (5) alone treated) based on 3-(4, 5-dimethyl 2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. In SHSY5Y cells, rotenone induced cytotoxicity, oxidative stress and mitochondrial dysfunction whereas pre-treatment of NPIASA attenuated the rotenone toxicity. Besides, rotenone induced the cytotoxicity by up-regulating caspases -3, -6, -8, -9 expressions and down regulating Bcl2 expression. NPIASA pre-treatment reversed the toxicity effects induced by rotenone in cells. Collectively, our results proposed that NPIASA mitigated the rotenone-induced oxidative stress, mitochondrial dysfunction and apoptosis. However, additionally pre-clinical studies are warranted in rodents to use NPIASA as a revitalizing therapeutic agent for PD in future.