Objective　To study the similarities and differences on in vitro replication and expression of hepatitis C virus (HCV) between human fetal hepatocytes (HFH) and 7721 cell line. Methods　Human fetal hepatocytes and a hepatoma cell line 7721 were incubated with a serum from hepatitis C patient. After incubation, the presence of HCV RNA, the expression of HCV NS3 antigens in cells and/or supernatant were examined by RT-PCR, in situ hybridization and immunohistochemistry, respectively. Results　It was found that: ①The intracellular HCV RNA was first detected on d 2～3 post-incubation and then could be intermittently detected in cells and/or supernatant subsequently (HCV RNA could be detected in 7721 cells during a period of at least 66 days. In HFH, HCV RNA could be detected up to 25 days after incubation); ②HCV-NS3 antigen could be expressed in infected cells; ③Minus-strand RNA of HCV was mainly located within cytoplasm by in situ hybridization. Conclusion　The results suggest that both the fetal hpatocytes and the hepatoma cell line 7721 are susceptible to HCV, and especially 7721 cell line can stably support HCV replication in vitro and may be used as the target cell for long-term cultures of HCV.

BACKGROUND: Pathological cardiac hypertrophy is one of the main activators of heart failure. Currently, no drug can completely reverse or inhibit the development of pathological cardiac hypertrophy. To this end, we proposed a silicate ion therapy based on extract derived from calcium silicate (CS) bioceramics for the treatment of angiotensin II (Ang II) induced cardiac hypertrophy. METHODS: In this study, the Ang II induced cardiac hypertrophy mouse model was established, and the silicate ion extract was injected to mice intravenously. The cardiac function was evaluated by using a high-resolution Vevo 3100 small animal ultrasound imaging system. Wheat germ Agglutinin, Fluo4-AM staining and immunofluorescent staining was conducted to assess the cardiac hypertrophy, intracellular calcium and angiogenesis of heart tissue, respectively. RESULTS: The in vitro results showed that silicate ions could inhibit the cell size of cardiomyocytes, reduce cardiac hypertrophic gene expression, including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and b-myosin heavy chain (b-MHC), decrease the content of intracellular calcium induced by Ang II. In vivo experiments in mice confirmed that intravenous injection of silicate ions could remarkably inhibit the cardiac hypertrophy and promote the formation of capillaries, further alleviating Ang II-induced cardiac function disorder. CONCLUSION This study demonstrated that the released silicate ions from CS possessed potential value as a novel therapeutic strategy of pathological cardiac hypertrophy, which provided a new insight for clinical trials.