肝硬化
CXCL10型
纤维化
肝星状细胞
医学
癌症研究
四氯化碳
MAPK/ERK通路
CXCL9型
下调和上调
肝纤维化
免疫学
趋化因子
炎症
信号转导
内科学
四氯化碳
生物
化学
基因
有机化学
生物化学
作者
Xiaoyun Guo,Yu Cen,Jiaxu Wang,Hai‐Xing Jiang
标识
DOI:10.1016/j.biopha.2018.05.128
摘要
Liver fibrosis is a typical complication of chronic liver diseases resulting in cirrhosis that remains a major public health problem. The aim of the present study was to identify the role of interleukin-9 (IL-9), an important regulator of inflammation and autoimmune diseases, in hepatic fibrosis progression. It was found that the expression of IL-9 was significantly increased in liver tissues of liver cirrhosis patients compared with that in healthy controls. Moreover, CXCL10, not CXCL9 or CXCL11, induced IL-9 expression in the liver tissue. Overexpression of IL-9 enhanced the severity of liver fibrosis in the carbon tetrachloride (CCl4)-induced liver fibrosis model. Western Blotting analysis revealed that this pro-fibrosis bioactivity of IL-9 was attributed to its selective activation of Raf/MEK/ERK signaling. Finally, administration of neutralizing anti-IL-9 antibody ameliorated liver fibrosis and attenuated the activation of hepatic stellate cells in mice. All these findings indicate that IL-9 plays a deleterious role in the development and progression of liver fibrosis, and IL-9 based immunotherapy may prove to be a promising strategy for the treatment of liver fibrosis.
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