Epigallocatechin-3-gallate (EGCG) attenuates concanavalin A-induced hepatic injury in mice

被引:49
作者
Liu, Dongmei [1 ]
Zhang, Xiaoli [1 ]
Jiang, Li [1 ]
Guo, Yun [1 ]
Zheng, Changqing [2 ]
机构
[1] China Med Univ, Shengjing Hosp, Dept Rheumatol & Immunol, Shenyang 110004, Peoples R China
[2] China Med Univ, Shengjing Hosp, Dept Gastroenterol, Shenyang 110004, Peoples R China
关键词
Hepatitis; Concanavalin A; Inflammation; Oxidative stress; Nuclear factor-kappa B; Toll-like receptors; Mice; NF-KAPPA-B; LIVER-INJURY; OXIDATIVE STRESS; AUTOIMMUNE HEPATITIS; POTENTIAL ROLE; TEA CATECHIN; T-CELLS; (-)-EPIGALLOCATECHIN-3-GALLATE; DISEASES; DAMAGE;
D O I
10.1016/j.acthis.2013.12.002
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
(-)-Epigallocatechin-3-gallate (EGCG) is the most abundant polyphenolic compound present in green tea and has been shown to possess anti-inflammatory and anti-oxidative properties. In this study, we investigated the protective effects of EGCG against concanavalin A (ConA)-induced liver injury and the underlying mechanisms. EGCG (5 mg/kg) was administered orally by gavage to mice twice daily for 10 days before an intravenous injection of ConA. We found that EGCG effectively rescued lethality, improved hepatic pathological damage, and decreased serum levels of alanine aminotransaminase (ALT) in ConA-challenged mice. Furthermore, EGCG also significantly prevented the release of tumor necrosis factor (TINF)-alpha, interferon (IFN)-gamma, interleukin (IL)-4, and IL-6 in serum, reduced malondialdehyde (MDA) levels, and restored glutathione (GSH) content and superoxide dismutase (SOD) activity in liver tissues from ConA-challenged mice. Finally, nuclear factor (NF)-kappa B activation and expression levels of Toll-like receptor (TLR) 2, TLR4 and TLR9 protein in liver tissues were significantly inhibited by EGCG pretreatment. Taken together, our data suggest that EGCG possesses hepatoprotective properties against ConA-induced liver injury through its anti-inflammatory and anti-oxidant actions. (C) 2013 Elsevier GmbH. All rights reserved.
引用
收藏
页码:654 / 662
页数:9
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