Protective effect of hypoxia inducible factor-1α on intestinal mucosal barrier in sepsis
10.12092/j.issn.1009-2501.2021.03.004
- Author:
Rui HE
1
;
Wenbin TENG
1
;
Shengmei ZHU
1
;
Liuxu YAO
2
;
Yue SHAN
2
;
Yuhong LI
3
Author Information
1. Department of Anesthesiology, the First Affiliated Hospital, College of Medicine, Zhejiang University
2. Department of Anesthesiology, Shaoxing People's Hospital
3. Shulan Hangzhou Hospital, Shulan International Medical College, Shuren University
- Publication Type:Journal Article
- Keywords:
Hypoxia inducible factor-1α;
Hypoxia inducible factor-1α inhibitor;
Hypoxia inducible factor-1α stimulant;
Inflammatory response;
Oxidative stress response;
Sepsis
- From:
Chinese Journal of Clinical Pharmacology and Therapeutics
2021;26(3):264-270
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To investigate the effect and mechanism of hypoxia inducible factor-1α on intestinal mucosal barrier in sepsis. METHODS: SD rats were randomly divided into 4 groups: sham group, sepsis group, sepsis+HIF-1α stimulant (sepsis+DMOG group), sepsis+HIF-1α inhibitor (sepsis+Bay87-2243 group), 6 rats in each group. Sepsis model was established by cecal ligation and perforation (CLP). The levels of inflammatory markers IL-1β, IL-6, TNF-α, oxidative stress markers MDA and antioxidant factors SOD and CAT were detected by ELISA and the expression of HIF-1α in intestinal mucosa was detected by Western blot. The pathological damage of intestinal mucosa was detected by HE staining. RESULTS: Inflammatory factors, oxidative stress factors and HIF-1α were significantly up-regulated in septic rats (P<0.05). The contents of IL-1β, IL-6, TNF-α and MDA in plasma were significantly decreased by intraperitoneal injection of DMOG (P<0.05); the levels of SOD and CAT in plasma were increased (P<0.05), HIF-1α was up-regulated (P<0.05), and the pathological damage of intestinal mucosa was alleviated, with decreased Chiu's score (P<0.05). Oral administration of Bay87-2243 gave the opposite result. CONCLUSION: HIF-1α has a protective effect on intestinal mucosal injury in sepsis. The mechanism may be related to the alleviation of inflammatory response and inhibition of oxidative stress.