The protective effect of glutamine pretreatment on intestinal ischemia-reperfusion injury and eNOS/NO levels in rats
10.3969/j.issn.0253-9896.2015.03.008
- VernacularTitle:谷氨酰胺预处理对大鼠肠缺血再灌注损伤的保护作用及其对eNOS-NO通路的影响
- Author:
Qiong NIU
;
Aili WANG
;
Wei WANG
;
Yingbin HU
;
Chengxia LIU
- Publication Type:Journal Article
- Keywords:
glutamine;
intestines;
ischemia;
reperfusion injury;
nitric oxide synthase;
intestinal ischemia-reperfusion
- From:
Tianjin Medical Journal
2015;(3):252-255
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effect of glutamine(Gln) pretreatment on intestinal ischemia-reperfusion (I/R) injury and endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) signaling pathway in rat model. Methods Thirty male Wistar rats were randomly divided into three groups(n=10 for each group):sham group, I/R group and Gln group. Animals were pretreated with 1 g/(kg·d)Gln by orogastric route for 7 days in Gln group, and normal saline was given to the other two groups in the same dose. Intestinal I/R was induced by 30 min occlusion of the superior mesenteric artery followed by 24 h of reperfusion. After the operation, the intestinal histopathological changes, the plasma endotoxin level, serum D-lactic acid, eNOS, inducible NOS(iNOS)activity and NO levels were detected by ultraviolet spectrophotometer. The mRNA expressions of myocardial eNOS and iNOS were detected by real-time fluorescence quantitative PCR (RT-PCR). Results After reperfusion, in IR group, extensive epithelial sloughing and mucosal ulceration of villous tips were observed, whereas these findings did not occur in Gln group and sham group. Compared with IR group, the serum NO, eNOS levels and eNOS mRNA expression of intestinal tissue were elevated in Gln group (P<0.01), but the plasma endotoxin level, serum D-lactic acid, serum iNOS and intestinal iNOS mRNA expression decreased in IR group(P<0.05). Conclusion Glutamine pretreatment has protective effects on intestinal ischemia-reperfusion injury in vivo. The mechanism may be related to the inhibition of iNOS expression and the increased expression of eNOS, thereby increasing NO activity.
