Effects of indoleamine 2,3-dioxygenases in carbon tetrachloride-induced hepatitis model of rats
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 a...
Gespeichert in:
Veröffentlicht in: | Cell biochemistry and function 2012-06, Vol.30 (4), p.309-314 |
---|---|
Hauptverfasser: | , , , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | 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‐α (TNF‐α) is critical in the development of liver injury. The mRNA expression and secretion levels of TNF‐α 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‐α and interleukin‐6. Copyright © 2012 John Wiley & Sons, Ltd. |
---|---|
ISSN: | 0263-6484 1099-0844 |
DOI: | 10.1002/cbf.2803 |