摘要

Background. Hepatic fibrosis is a reversible pathological process. Inflammatory responses are the prevailing reactions during hepatic fibrosis. Decoy receptor 3 (DcR3) has been reported to have an anti-inflammatory effect. @@@ Objectives. The aim of the study was to investigate the preventive effects of DcR3 on hepatic fibrosis. @@@ Material and methods. Hepatic fibrosis was induced in rats by administering intraperitoneally (ip.) 1% dimethylnitrosamine (DMN). DcR3 plasmid was delivered into rats by intravenous injection. After 4 weeks, the expression of DcR3, TNF-like molecule 1A (TL1A) and alpha-SMA of the liver tissue were checked. The levels of inflammatory cytokines such as TNF-alpha, IL-6 and IL-1 beta were detected using western blotting and quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR). Masson's trichrome staining for histopathological changes of the liver tissue was observed. Finally, the activity of NF-kappa B in the liver was examined by enzyme-linked immunosorbent assay (ELISA). @@@ Results. A higher expression of DcR3 was observed in rats treated with DcR3 (p < 0.05). Histological results showed that DcR3 significantly attenuated pathology in hepatic fibrosis rats. Consistently, mRNA and protein levels of alpha-SMA, TL1A, TNF-alpha, IL-6, and IL-1 beta were repressed in the liver tissue after treatment with DcR3 (p < 0.05). Moreover, DcR3 also inhibited the activation of NF-kappa B in the liver tissue (p < 0.05). @@@ Conclusions. This study demonstrated that DcR3 attenuated liver injury and inflammatory responses in rats with hepatic fibrosis. We suggest DcR3 may be a prophylactic and promising therapeutic agent in the treatment of hepatic fibrosis.