Expression of TRIF of innate immunity signal pathway in hepatic fibrosis
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KeyWord:Hepatic fibrosis; Innate immunity; TOLL-like receptors; TIR-domain-containing adapter-inducing interferon-β (TRIF); Rat
黄欣 重庆医科大学中医药学院,重庆
李艳 重庆医科大学中医药学院,重庆
贺雄 重庆医科大学中医药学院,重庆
赵苹利 重庆医科大学中医药学院,重庆
曹文富 重庆医科大学中医药学院,重庆
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      Objective To study the characteristics of expression of TRIF (TIR-domain-containing adapter-inducing interferon-β, TRIF) innate immune signaling factors in hepatic cells and its protein expression pattern in hepatic fibrosis in rats, and to explore the relationship between the important signal downstream of TOLL-like receptor TRIF and pathogenetic mechanism of hepatic fibrosis. Methods To generate rat models of hepatic fibrosis by subcutaneous injection of carbon tetrachloride together with low protein and high fat diet and alcohol water drinking. Thirty two SD rats were randomly divided into control group and model group. Intracardiac saline and formaldehyde fixative perfusion was performed in some rats and liver tissue samples were taken for histopathological and immunohistochemical examination. Other rats were killed by direct decapitation and fresh liver tissue samples were taken for electron microscopic examination and Western blot assay. Results The HE staining showed that normal rat liver displaying regular lobular structure without inflammatory cell infiltration, but the model rat livers showed distinct disordered lobular structure, decreased amount of hepatocytes and the presence of hepatic fobrosis. Electron microscopic observation revealed deposition of collagen fibers and cytolysis of hepatocytes, karyolysis of Kuppfer cells, cytolysis of sinusoidal endothelial cells and a large number of abnormal cells infiltration. Immunohistochemistry showed a high expression of TRIF in endothelial and stellate cells, mainly, in the cell nuclei, but also could be seen in the cytoplasm. Compared with the normal control group, the TRIF protein expression was significantly increased in the model rat livers (P<0.01), consistent with that observed by histopathology. ConclusionsTRIF expression is significantly increased in liver fibrosis, indicating an apparent activation of Toll-like receptor and a series of immunological responses via the downstream signal transduction pathways, producing a series of in vivo immune responses. It is preliminarily confirmed that the innate immune signal factor TRIF plays an important role in the pathogenesis of hepatic fibrosis.
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