Effect of N-acetylcysteine on intestinal injury induced by cardiopulmonary bypass in rats.
- Author:
Zhiyang XU
1
;
Guoying JIANG
;
Shiqing LIN
;
Jun GUAN
;
Guodu CHEN
;
Guanze CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Acetylcysteine; pharmacology; Animals; Cardiopulmonary Bypass; adverse effects; Glutathione; metabolism; Glutathione Peroxidase; metabolism; Inflammation; drug therapy; Interleukin-6; metabolism; Intestines; drug effects; physiopathology; Malondialdehyde; metabolism; Oxidative Stress; drug effects; Rats; Superoxide Dismutase; metabolism; Tumor Necrosis Factor-alpha
- From: Journal of Southern Medical University 2014;34(8):1171-1175
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of N-acetylcysteine (NAC) on intestine injury induced by cardiopulmonary bypass (CPB) in rats.
METHODSThirty-two rats were randomly divided into sham-operated group, NAC control group, CPB model group, and CPB plus NAC treatment group (n=8). In the latter two groups, the rats were subjected to CPB for 1 h. The rats received intraperitoneal injections of normal saline or NAC (0.5 g/kg) as appropriate for 3 successive days prior to CPB, and those in CPB plus NAC group were given NAC (100 mg/kg) in CPB prime followed by infusion at 20 mgsol;(kg·h) until the cessation of CPB. Intestinal and blood samples were collected 2 h after CPB for pathological analysis and measurement of intestinal concentrations of malondialdehyde (MDA), tumor necrosis factor (TNF)-α, interlukin (IL)-6 and activity of superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GSH-Px) and serum levels of diamine oxidase (DAO).
RESULTSEvident oxidative stress and pathological damages of the intestines were observed in rats after CPB. NAC treatment obviously alleviated intestinal damages induced by CPB, decreased the levels of intestinal MDA, TNF-α, IL-6 and serum DAO and increased activity of SOD, GSH, and GSH-Px in the intestines.
CONCLUSIONPerioperative NAC treatment can alleviate intestinal injury induced by CPB in rats by suppressing oxidative stress and inflammatory response.