AI Article Synopsis
- - The study investigated how the absence of indoleamine 2,3-dioxygenase (IDO) affects liver fibrosis caused by carbon tetrachloride (CCl4).
- - IDO-deficient mice (IDO-KO) showed worse liver damage and higher levels of inflammatory cells and cytokines compared to normal mice (WT) after CCl4 treatment.
- - Additionally, introducing l-tryptophan worsened liver fibrosis in WT mice, demonstrating that IDO deficiency increases liver inflammation and fibrosis in response to repeated CCl4 exposure.
Article 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.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5012673 | PMC |
| http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0162183 | PLOS |
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