Changes of iNOS genes expression in liver following ischemia and reperfusion of limbs and their significance in rats.
- Author:
Zhong-li SHI
1
;
Yi-ling LING
;
Yu-xia YAO
;
Jun-lin ZHOU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Guanidines; pharmacology; Hindlimb; blood supply; Liver; blood supply; metabolism; Male; Malondialdehyde; analysis; Nitric Oxide; metabolism; Nitric Oxide Synthase Type II; metabolism; Rats; Rats, Sprague-Dawley; Reperfusion Injury; metabolism; Superoxide Dismutase; analysis
- From: Chinese Journal of Applied Physiology 2004;20(2):172-175
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo detect the changes of inducible nitric oxide synthase (iNOS) expression in liver following ischemia/reperfusion (I/R) of hindlimbs and to elucidate their significance.
METHODSI/R was established using the occlusion of the femoral arteries for 4 h and reopening for 2-24 h in rats. The expression of iNOS mRNA, and iNOS protein and the nitrotyrosine (NT), a marker of peroxynitrite (ONOO-), in liver tissue were detected with reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical technique, respectively. The liver superoxide dismutase (SOD) activity and malondialdehyde (MDA) contents were spectrophotometrically measured. The observation of pathologic changes of liver was made following the inhibition of iNOS by aminoguanidine (AG).
RESULTSCompared with control groups, the relative expression level of iNOS mRNA significantly increased in I/R group. There were more iNOS positive hepatocytes and more NT positive hepatocytes in I/R group than control groups. The contents of MDA markedly increased, while the activity of SOD significantly decreased in I/R group, compared with those in the control groups. The pathologic changes of rat liver became milder in I/R group following the inhibition of iNOS by AG.
CONCLUSIONThe expressions of iNOS mRNA and protein in liver are significantly upregulated, excess induction of iNOS-NO is contributed to the liver injury during the I/R of hindlimbs.