The purpose of this study was to examine the consequences of opening KATP channels using nicorandil in an in vitro 6-OHDA Parkinsons disease model conducted in SH-SY5Y cells. To establish Parkinsons disease model in vitro, 200µM 6-OHDA administered to the cells for 24h. Half an hour before the 6-OHDA administration, SH-SY5Y cells were pre-treated with nicorandil (10, 100, 500 and 1000µM). After 1 day, cell viability was determined with the 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) and lactate dehydrogenase (LDH) assays. Oxidative stress was assessed with superoxide dismutase (SOD), glutathione (GSH), reactive oxygen species (ROS) and malondialdehyde (MDA) analyses. We found that 6-OHDA increased LDH leakage, and cellular apoptosis in SH-SY5Y cells. 6-OHDA aggravated oxidative stress by increasing ROS and MDA and eventually promoted apoptosis by increasing mRNA expression levels of Caspase-3 in SH-SY5Y cells, while pretreatment with nicorandil attenuated these toxic effects of 6-OHDA by suppressing oxidative stress and apoptosis. Considering its neuroprotective role in addition to its effects on oxidative stress and apoptosis, nicorandil may be a useful agent in the treatment of Parkinsons disease.
Key words: Nicorandil, KATP, 6-OHDA, parkinsons disease, SH-SY5Y
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