Protective effects of epigallocatechin-3-gallate on intestinal ischemia reperfusion injury through enhanced activation of PI3K/Akt pathway in rats.
10.1007/s11596-015-1441-2
- Author:
Xuan ZHANG
1
;
Fan HE
;
Jun YANG
;
Zhi-Shui CHEN
Author Information
1. Key Laboratory of Organ Transplantation, Ministry of Education and Ministry of Public Health, Institute of Organ Transplantation, Wuhan, 430030, China, zhangxuantj@163.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Anti-Inflammatory Agents;
administration & dosage;
pharmacology;
Catechin;
administration & dosage;
analogs & derivatives;
pharmacology;
Disease Models, Animal;
Gene Expression Regulation;
drug effects;
Interleukin-1;
genetics;
metabolism;
Interleukin-6;
genetics;
metabolism;
Intestines;
drug effects;
pathology;
Male;
Phosphatidylinositol 3-Kinases;
metabolism;
Proto-Oncogene Proteins c-akt;
metabolism;
Rats;
Rats, Wistar;
Reperfusion Injury;
genetics;
metabolism;
prevention & control;
Signal Transduction;
drug effects;
Tumor Necrosis Factor-alpha;
genetics;
metabolism
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2015;35(3):378-383
- CountryChina
- Language:English
-
Abstract:
Inflammation plays a critical role in intestinal ischemia reperfusion injury (IRI). Epigallocatechin-3-gallate (EGCG) has been demonstrated to possess anti-inflammatory effect. This study examined the effect of EGCG on intestinal IRI and explored the possible mechanisms. Male Wistar rats were randomly divided into three groups: sham-operated group (Sham), IRI control group (IRI) and IRI-EGCG group (EGCG). Rats in IRI-EGCG group were administered dissolved EGCG in drinking water (0.4 mg/mL) for 14 days prior to IRI induction. A rat model of intestinal IRI was established by ligating the superior mesenteric artery (SMA) for 30 min, followed by reperfusion for 1 h. Intestinal histology, pro-inflammatory cytokines and mediators were examined and the effect of EGCG on PI3K/Akt signalling was assessed. EGCG significantly alleviated the pathological changes of the intestine and suppressed the IRI-induced up-regulation of TNF-α, IL-1 and IL-6 mRNA and protein expression in the serum and intestine. The mechanism might be that EGCG enhanced the activation of PI3K/Akt signalling pathway. In conclusion, the administration of EGCG can significantly mitigate the acute intestinal IRI in rats by enhancing the activation of PI3K/Akt signalling pathway to suppress inflammatory response and might be a promising alternative for the prevention or treatment of intestinal IRI in the clinical practice.
