Neuroprotective Effects of Nicorandil in Chronic Cerebral Hypoperfusion-Induced Vascular Dementia.

摘要: Background Ischemia-induced chronic cerebral hypoperfusion (CCH) is associated with reduced blood flow and vascular dementia (VaD). Brain mitochondrial potassium (adenosine triphosphate-sensitive [K ATP ]) channels have a beneficial role in various brain conditions. The utility of K CCH-induced VaD still unknown. aim this study to investigate the nicorandil, selective channel opener, VaD. Methods method 2-vessel occlusion (2VO) was used induce CCH mice. Cognitive impairment assessed using Morris water maze. Serum nitrosative stress (nitrite/nitrate), cholinergic dysfunction (acetylcholinesterase [AChE] activity), oxidative (thiobarbituric acid reactive substances, glutathione [GSH], catalase [CAT], superoxide dismutase [SOD]), inflammation (myeloperoxidase [MPO]), infarct size (2,3,5-triphenyltetrazolium chloride staining) were assessed. Results 2-vessels-occluded animals shown significant cognitive impairment, serum (reduced nitrite/nitrate), (increased AChE increased (reduction GSH content SOD CAT activities increase lipid peroxidation), along MPO activity size. However, nicorandil treatment has significantly attenuated behavioral biochemical impairments. Conclusions It may be said that 2VO provoked leading VaD, which by nicorandil. So, modulation provide benefits