Type: dissertation
Abstract: Purpose: Nitrite-derived NO has been shown to provide neuroprotection against brain ischemia-reperfusion injury.The present study was designed to examine the effect and mechanism of nitrite-derived NO on cerebral infarct volume in a chronic rat model.Methods: Male Sprague-Dawley rats were divided into eight treatment groups : saline only, three groups with different doses of sodium nitrite (NaNO2), L-NNA (NOS inhibitor) with saline and with NaNO2, ODQ (soluble guanylate cyclase inhibitor) with saline and with NaNO2, C-PTIO (NO scavenger) with saline and with NaNO2, allopurinol (xanthine oxidase inhibitor) with saline and with NaNO2, indomethacin (COX inhibitor) with saline and with NaNO2, and U-51605 (prostacyclin synthase inhibitor) with saline and with NaNO2.The rat was injected intraperitoneally with one of the above combinations, followed by one-hour occlusion of the middle cerebral artery and then by reperfusion.Five days later, the brain was stained for quantification of cerebral infarction area as percentage of the whole brain area.Results: Nitrite significantly reduced the cerebral infarct area in a dose-dependent manner.The nitrite-induced reduction in cerebral infarct area was unaffected in rats injected with C-PTIO, ODQ, allopurinol, indomethacin and U-51605.However, injection of L-NNA augmented the reduction in nitrite-induced cerebral infarct area.Conclusion: Nitrite-derived NO protects the brain against ischemia-reperfusion injury through NOS-independent but GC/COX/xanthine oxidase/PGIS-dependent pathways.-ⅲ-目次 頁
Author: ANDO, Hisae
Language: English
Subfield: Physiology (medical)
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W7163619968