Expression of iNOS protein and gliacyte apoptosis in neonatal rats with white matter damage.
- Author:
Hui-Qing WANG
1
;
Ying XIONG
;
Wen-Jun GUO
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Animals, Newborn; Apoptosis; Brain; pathology; Hypoxia-Ischemia, Brain; metabolism; pathology; In Situ Nick-End Labeling; Leukoencephalopathies; metabolism; pathology; Neuroglia; pathology; Nitric Oxide; physiology; Nitric Oxide Synthase Type II; analysis; physiology; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Contemporary Pediatrics 2011;13(4):309-312
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVEInducible nitric oxide synthase (iNOS) is a main rate-limiting enzyme resulting in over-production of nitric oxide following hypoxia-ischemia (HI). The aim of this study was to observe the expression of iNOS protein and gliacyte apoptosis in the brains of premature rats after HI, in order to explore possible relationships of iNOS with white matter damage (WMD).
METHODSOne hundred and twelve 2-day-old premature rats were randomly subjected to right carotid ligation followed by 4 hrs hypoxic stress (WMD group) or sham operation (control group). The pups were sacrificed at 1, 3, 6, 12 hrs, and 1, 3 and 7 days after HI. Immunohistochemical technique was applied to determine the iNOS expression in periventricular white matter tissues. Gliacyte apoptosis was detected in these tissues by TUNEL.
RESULTSCompared with the control group, iNOS expression began to increase 1 hr after HI and reached the peak 1 day after HI in the WMD group. Gliacyte apoptosis increased 1 hr after HI and peaked 1 day after HI in the WMD group compared with the control group.
CONCLUSIONSIn the neonatal rats with WMD, the expression of iNOS may be involved in the ischemic cellular events including apoptosis, and plays a role in the pathophysiological process of WMD.
