Objective: The aim of this study is to explore the relationships among miR-200a expression, hepatic fibrosis, and liver inflammation of Biliary Atresia (BA) in mice.
Methods: Newly born Balb/c mice received intraperitoneal injection with rhesus monkey rotavirus. The BA model of mice was established. The mice were killed 4, 8, 14, and 21 d after the injection. The normal control group received intraperitoneal injection with equal volume of virus culture solution. Blood samples from the experimental groups were collected before killing, and liver tissues were obtained through laparotomy. Alanine Aminotransferase (ALT), Aspartate Aminotransferase (AST), Serum Hyaluronic Acid (HA), Layer Fibronectin (LN), Procollagen III (PCIII), and Collagen type IV (CIV) contents were tested by a biochemical analyzer.
Results: All the experimental groups showed higher ALT, AST, HA, LN, PCIII, CIV, IL-6, and TNF-α contents than the normal control group (P<0.05). No significant change in CIV concentration was observed after 14 and 21 d. Significant difference was observed among the CIV concentrations of the experimental groups (P<0.05). Different experimental groups have different degrees of hepatic fibrosis and inflammation. Compared with the control group, the experimental groups had more severe hepatic fibrosis (P<0.05). Statistical significance was observed among the experimental groups (P<0.05). The relative expression levels of miR-200a mRNA of the experimental groups were significantly higher than that of the control group (P<0.05).
Conclusions: The relative expression of miR-200a mRNA in the liver tissues of virus-induced BA mice model is upregulated significantly. Therefore, miR-200a participate in the generation and development of hepatic fibrosis and liver inflammation in mice with BA.