Protective effects of Epigallocatechin gallate on liver ischemia reperfusion injury in rats
10.3760/cma.j.issn.1007-8118.2018.03.014
- VernacularTitle:儿茶素没食子酸酯预处理对大鼠肝脏缺血再灌注损伤的保护作用
- Author:
Xiao LI
1
;
Xuan ZHANG
;
Quancheng WANG
;
Hong ZHANG
;
Ge BAI
;
Kaishan TAO
;
Kefeng DOU
Author Information
1. 第四军医大学西京医院肝胆外科
- Keywords:
Liver;
Ischemia reperfusion injury (IRI);
Epigallocatechin gallate (EGCG);
Signal transduction,PI3K/AKT;
Inflammatory cytokine
- From:
Chinese Journal of Hepatobiliary Surgery
2018;24(3):199-203
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective roles of Epigallocatechin gallate (EGCG) on liver ischemia reperfusion injury (IRI) in rats.Methods 30 healthy male SD rats were selected and equally and randomly divided into 3 groups.Sham group,IRI group and IRI-EGCG group were established to construct 70％ liver IRI rat model.Drinking water with 0.4 mg/ml EGCG was administered for 2 weeks before the experiment in IRI-EGCG group.HE staining was performed to evaluate the injury.Transaminases in serum were investigated to assess liver injury.p-p85 and p-AKT was detected by Western-blot assay.qPCR was carried out to study the mRNA expression of TNF-α,IL-6 and IL-1β in liver tissue.The secretion of TNF-α,IL-6 and IL-1 β in serum was examined with ELISA assay.Results EGCG pretreatment reduced ASTand ALT in serum [AST:(550.0 ±66.5) IU/L vs.(220.0 ±63.5) IU/L;ALT:(376.0 ± 25.7) IU/L vs.(158.0 ± 33.1) IU/L,all P ＜ 0.05] and mitigated liver tissue damage.p-p85 and p-AKT increased due to liver IRI,and IRI-EGCG group showed higher expression of p85 and AKT.The proinflammatory cytokines of TNF-α,IL-6 and IL-1 β exhibited a relatively lower mRNA expression in IRI-EGCG group comparing with IRI group.IRI-EGCG group also revealed a decreased secretion of TNF-α,IL-6 and IL-1β in serum [TNF-α:(398.0±33.4) ng/Lvs.(211.0±23.6) ng/L;IL-6:(341.0±27.3) ng/L vs.(187.0±19.6) ng/L;IL-1β:(486.0±43.7) ng/L vs.(352.0±31.5) ng/L;allP＜0.05].Conclusion EGCG pretreatment can enhance IRI-induced activation of PI3K/AKT signaling and reduce the release of proinflammatory cytokines to exert liver protective effects.
