Effects of indoleamine 2,3-dioxygenases in carbon tetrachloride-induced hepatitis model of rats

被引:10
|
作者
Li, Dan [1 ]
Cai, Haidong [1 ]
Hou, Min [1 ]
Fu, Da [1 ]
Ma, Yushui [1 ]
Luo, Qiong [1 ]
Yuan, Xueyu [1 ]
Lv, Mingli [1 ]
Zhang, Xiaoping [1 ]
Cong, Xianling [2 ]
Lv, Zhongwei [1 ]
机构
[1] Tongji Univ, Sch Med, Shanghai Peoples Hosp 10, Dept Nucl Med, Shanghai 200072, Peoples R China
[2] Jilin Univ, China Japan Union Hosp, Dept Dermatol, Changchun 130031, Peoples R China
基金
中国博士后科学基金;
关键词
CCl4; IDO; 1-MT; Liver; TNF; IL-6; T-CELL PROLIFERATION; INDUCED LIVER-INJURY; TRYPTOPHAN CATABOLISM; ALPHA-GALACTOSYLCERAMIDE; IN-VIVO; UP-REGULATION; TNF-ALPHA; MICE; INHIBITION; HEPATOCYTE;
D O I
10.1002/cbf.2803
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Indoleamine 2,3-dioxygenase (IDO) converts tryptophan to l-kynurenine, and it is noted as a relevant molecule in promoting tolerance and suppressing adaptive immunity. In this study, to investigate the effects of IDO in carbon tetrachloride (CCl4)induced hepatitis model, the levels of IDO enzymic activities in the mock group, the control group and the 1-methyl-d-tryptophan (1-MT)treated group were confirmed by determination of l-kynurenine concentrations. Serum alanine aminotransferase levels in 1-MT-treated rats after CCl4 injection significantly increased compared with those in mock and control groups. In CCl4-induced hepatitis models, tumour necrosis factor-a (TNF-a) is critical in the development of liver injury. The mRNA expression and secretion levels of TNF-a in the liver from 1-MT-treated rats were more enhanced compared with those in the mock and the control groups. Moreover, the levels of cytokine and chemokine from mock, control group and 1-MT-treated rats after treated with CCl4 were analyzed by ELISA, and the level of interleukin-6 was found to increase in 1-MT-treated rats. It was concluded that the deficiency of IDO exacerbated liver injury in CCl4-induced hepatitis and its effect may be connected with TNF-a and interleukin-6. Copyright (c) 2012 John Wiley & Sons, Ltd.
引用
收藏
页码:309 / 314
页数:6
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