Inducible nitric oxide synthase and brain hypoxic-ischemic brain damage.
- Author:
Hai-Ting LIU
1
;
De-Zhi MU
Author Information
1. Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu 610041, China. liuhaiting9@163.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Humans;
Hypoxia-Ischemia, Brain;
drug therapy;
metabolism;
Nitric Oxide Synthase Type II;
antagonists & inhibitors;
genetics;
physiology
- From:
Chinese Journal of Contemporary Pediatrics
2014;16(9):962-967
- CountryChina
- Language:Chinese
-
Abstract:
Brain hypoxia-ischemia has been considered as critical factors in many human central nervous system diseases, including stroke and neonatal hypoxic-ischemic encephalopathy. In brain hypoxia-ischemia processes, inducible NO synthase (iNOS) is induced to produce excessive nitric oxide (NO) which leads to cascade reactions of inflammation and neuronal death, deteriorating primary brain injury. Inhibiting iNOS expression has opened new perspectives in the treatment of brain hypoxia-ischemia because iNOS inhibitor has been shown as a potent therapeutic agent. This reviews focus on recent research achievements regarding the relationship between iNOS and ischemic-hypoxic brain damage and the perspective of using iNOS inhibitors as therapeutic strategies for brain ischemic-hypoxic brain damage.
