Abstract
In the present study, we examined the role of indoleamine 2,3-dioxygenase (IDO) in the development of CCl4-induced hepatic fibrosis. The liver fibrosis induced by repetitive administration with CCl4 was aggravated in IDO-KO mice compared to WT mice. In IDO-KO mice treated with CCl4, the number of several inflammatory cells and the expression of pro-inflammatory cytokines increased in the liver. In the results, activated hepatic stellate cells (HSCs) and fibrogenic factors on HSCs increased after repetitive CCl4 administration in IDO-KO mice compared to WT mice. Moreover, the treatment with l-tryptophan aggravated the CCl4-induced hepatic fibrosis in WT mice. Our findings demonstrated that the IDO deficiency enhanced the inflammation in the liver and aggravated liver fibrosis in repetitive CCl4-treated mice.
Highlights
Hepatic fibrosis is a wound-healing response to various chronic hepatic injuries resulting from viral infection, alcohol abuse, drugs, metabolic diseases, or autoimmune diseases [1]
We examined the effect of IDO on carbon tetrachloride (CCl4)-induced liver fibrosis in mice and demonstrated that the deficiency of IDO aggravates the development of liver fibrosis
We found that hepatic fibrosis in IDO-KO mice was exacerbated by repeated administration of CCl4 compared to that in WT mice
Summary
Hepatic fibrosis is a wound-healing response to various chronic hepatic injuries resulting from viral infection ( hepatitis B and C), alcohol abuse, drugs, metabolic diseases, or autoimmune diseases [1]. Continued progression of hepatic fibrosis results in liver cirrhosis and may cause chronic hepatic failure or liver cancer [2]. The most important event in hepatic fibrosis is the activation of hepatic stellate cells (HSCs). Following liver injury of any etiology, HSCs undergo a response activation, which involves the transition of quiescent cells into proliferative and fibrogenic myofibroblasts. Such activated HSCs are able to produce ECM in the liver [1]
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