关键词: 日本血吸虫病, 肝纤维化, 转化生长因子, 受体, 治疗

Abstract: 　Objective To investigate the effect of interferon-γ(IFN-γ)on the expression of TGF-β1 and its two membrane receptors - TGF-β receptor I(TβRI), TGF-β receptor II(TβRII), and observe the expression of TGF-β1, TβRI and TβRII during the development of liver fibrosis in BALB/c mice infected by Schistosoma japonicum. Methods BALB/c mice, aged 6-8 weeks, were infected with cercariae of S. japonicum. The infected mice were divided randomly into three groups 16 week after infection:model group,praziquantel group and praziquantel combined with IFN-γ group. Liver specimen were obtained at 8, 12, 16 week and at the end of treatment. Pathological examination, immunohistochemistry and RT-PCR were used to evaluate the pathological change, the expression of TGFβ1, TβRI and TβRII and the mRNA level respectively. Results The expression of TGF-β1, TβRI, and TβRII can be detected in infected mice, while the expression around egg granulomas enhanced along with the progress of the disease. With the therapy of IFN-γ, the reduction of egg granulomas, and of the expression of TGF-β1, TβRI and TβRII was observed. From the transcription level, it was found that TGF-β1 mRNA increased at 12 week and peaked at model group, then decreased to the normal level after treatment with IFN-γ combined with praziquantel. The level of TβRII mRNA reduced at 8 and 16 week and returned to normal at the end of treatment. More interestingly, TβRI mRNA remained at the normal level on the whole course both in the development of fibrogenesis and the period of treatment. Conclusion The up regulation of TGFβ1 and down regulation of TβRII mRNA may induce liver fibrogenesis and IFN-γ might suppress TGFβ1 to reverse fibrosis. The mechanism of the suppression is mediated by down regulation of expression of its two receptors at protein level but not by influencing the mRNA expression.

Key words: Schistosomiasis japonica, Liver fibrosis, Transforming growth factor-β1, Receptor, Therapy