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The Deficiency of Indoleamine 2,3-Dioxygenase Aggravates the CCl(4)-Induced Liver Fibrosis in Mice

In the present study, we examined the role of indoleamine 2,3-dioxygenase (IDO) in the development of CCl(4)-induced hepatic fibrosis. The liver fibrosis induced by repetitive administration with CCl(4) was aggravated in IDO-KO mice compared to WT mice. In IDO-KO mice treated with CCl(4), the number...

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Detalles Bibliográficos
Autores principales: Ogiso, Hideyuki, Ito, Hiroyasu, Ando, Tatsuya, Arioka, Yuko, Kanbe, Ayumu, Ando, Kazuki, Ishikawa, Tetsuya, Saito, Kuniaki, Hara, Akira, Moriwaki, Hisataka, Shimizu, Masahito, Seishima, Mitsuru
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5012673/
https://www.ncbi.nlm.nih.gov/pubmed/27598994
http://dx.doi.org/10.1371/journal.pone.0162183
Descripción
Sumario:In the present study, we examined the role of indoleamine 2,3-dioxygenase (IDO) in the development of CCl(4)-induced hepatic fibrosis. The liver fibrosis induced by repetitive administration with CCl(4) was aggravated in IDO-KO mice compared to WT mice. In IDO-KO mice treated with CCl(4), 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 CCl(4) administration in IDO-KO mice compared to WT mice. Moreover, the treatment with l-tryptophan aggravated the CCl(4)-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 CCl(4)-treated mice.