Protective Effects of Epigallocatechin-3-gallate on Intestinal Ischemia Reperfusion Injury through Enhanced Activation of PI3K/Akt Pathway in Rats
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...
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Veröffentlicht in: | Journal of Huazhong University of Science and Technology. Medical sciences 2015-06, Vol.35 (3), p.378-383 |
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Sprache: | eng |
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Zusammenfassung: | 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/m L) 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 m RNA 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. |
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ISSN: | 1672-0733 1993-1352 |
DOI: | 10.1007/s11596-015-1441-2 |