中文摘要：

目的：研究长效干扰素人血清白蛋白融合干扰素（HSA-IFNd2b）对HepG2．2．15细胞增殖、凋亡及其HBsAg与HBeAg表达的影响，探讨其体外抑制乙肝病毒的机制。方法：采用SRB法分析HsA_IFNa2b作用HepG2．2．15细胞3，6d后对其增殖的影响，酶联免疫分析不同剂量HsA_IFNd2b作用不同时间后HepG2．2．15细胞HBsAg与HBeAg的表达水平，Hochest33342、PI双染法观察细胞的凋亡和死亡，WesternBlot印迹检测Bcb2、Bax的表达。结果：HepG2．2．15细胞的增殖在加HsA-IFNa2b作用3，6d后都有所抑制，细胞培养上清中HBsAg表达明显下降，并与浓度相关，HsA_IFNQ2b浓度为10000U·mL^-1时，培养6d后HBsAg的抑制率达87％以上。Hochest33342、PI双染结果显示当HSA．IFNa2b浓度在1250U·mL^-1。时可见少量的凋亡细胞，凋亡细胞数随着药物浓度的增大而增多，并有少量死亡细胞出现。WesternBlot印迹检测随药物浓度的增加Bcl-2的表达降低而BaX的表达增加。结论：HSA-IFNa2b体外可明显抑制HepG2．2．15细胞的增殖及HB—sAg的表达，并可引起HepG2．2．15细胞的凋亡和死亡。

英文摘要：

OBJECTIVE To evaluate the effects of a long-acting interferon （HSA-IFNa2b） on the proliferation, apoptosis and expression of HBsAg and HBeAg in HepG 2.2. 15 cells, and to investigate the mechanism of inhibition of hepatitis B virus in vitro. METHODS The cells proliferation was determined by SRB method. The expression levels of HBsAg and HBeAg in supernatant were measured using enzyme-linked dimmunosorbent assay （ELISA）. Apoptosis and death were observed by Hochest33342 and PI double staining. Expression of Bcl-2 and Bax proteins were determined with Western blot. RESULTS The results demonstrated that HSA-IFNa2b could inhibit the proliferation of HepG 2. 2. 15 cells. The expression of HBsAg in HepG 2. 2.15 cells was inhibited by HSA-IFNa2b in a time and dose-dependent manner. Treated with 10 000 u.mL^-1 HSAIFNa2b for six days, the inhibitiory rates of HBsAg was above 87%. The Results of Hochest33342 and PI double staining demonstrated HSA-IFNa2b could induce the apoptosis of HepG 2. 2. 15 cells in a dose-dependent manner. The cell death was also occurred at the higher concentration of HSA-IFNa2b. The results of Western blot analysis showed that HSA-IFNa2b could inhibit the expression of Bcl-2, while enhance the expression of Bax. CONCLUSION HSA-IFNa2b could not only significantly inhibit the HBsAg expression and the proliferation of HepG 2. 2. 15 cells, but also induced the apoptosis and death.