TY  - JOUR
TI  - Neuroprotective effect of nicorandil in 6-OHDA induced in vitro model of
parkinson's disease
AB  - The purpose of this study was to examine the consequences of opening KATP channels using nicorandil in an in vitro 6-OHDA Parkinson’s disease model conducted
in SH-SY5Y cells. To establish Parkinson’s 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 Parkinson’s disease.
AU  - Okkay, Ufuk
AU  - Ferah Okkay, Irmak
DO  - 10.5455/medscience.2021.07.231
PY  - 2022
JO  - Medicine Science
VL  - 11
IS  - 1
SN  - 2147-0634
SP  - 224
EP  - 227
DB  - TRDizin
UR  - http://search/yayin/detay/522759
ER  -