Objective:To investigate the effect and role of the hepatitis B virus (HBV) on the expression of inhibin (PHB) in the proliferation and survival of hepatocellular carcinoma (HCC) cells.Methods:The expression of PHB in 13 pairs of HBV-infected livers, normal livers and HepG2.2.15 and HepG2 cells was detected by real-time fluorescent quantitative PCR and Western blot. Liver tissues were collected from seven patients with chronic hepatitis B before and after antiviral (tenofovir) treatment, and the expression of PHB was detected by RT-PCR and Western blot. HepG2.2.15 cells were transfected with Pcmv6-AC-GFP-PHB, and control vectors were collected. DNA content was analyzed by flow cytometry. The proliferation level of each cell group was detected using the EdU cell proliferation assay. HepG2.2.15 cells transfected with Pcmv6-AC-GFP-PHB and the control vector were cultured in serum-free medium for 6 days. Apoptosis was measured at the indicated time points using fluorescence-activated cell sorting (FACS)-based Annexin-V/PI double staining.Results:Compared with normal liver tissue, the expression of PHB in HBV-infected liver tissue was down-regulated ( P < 0.01). Compared with HepG2 cells, the expression of PHB in HepG2.2.15 cells was significantly decreased ( P < 0.01). The expression level of PHB in liver tissue after antiviral treatment (tenofovir) was significantly higher than that before treatment ( P < 0.01). Compared with the control vector, the proliferation rate of HepG2.2.15 cells transfected with Pcmv6-AC-GFP-PHB was significantly lower than that of the control vector, and the apoptosis rate of HepG2.2.15 cells transfected with the Pcmv6-AC-GFP-PHB vector was significantly higher than the control vector ( P < 0.01). Conclusion:HBV down-regulates the expression of inhibin to promote the proliferation and survival of hepatocellular carcinoma cells.

Objective: To investigate the differential expression of serum-and-glucocorticoid-inducible-kinase-2 (SGK2) in hepatocellular carcinoma (HCC) and normal liver tissues and the related mechanism mediating signal transduction of GSK-3 β / β catenin in HCC cells. Methods: Twenty pairs of matched HCC and normal tissues were collected and the situation of expression of SGK2 mRNA was detected by real-time fluorescence quantitative PCR. Western blot was used to detect the levels of SGK2 protein in human HCC cell lines (Huh-7, SMMC-7721) and normal human liver cell line (L02). SGK2 siRNA was used to transfect human HCC cell lines (SMMC-7721 and Huh-7), and then the protein expression levels of GSK-3 β/ β - catenin was successfully detected with the above-mentioned transfected cell line by western blot. Measurement data were expressed as mean ± standard deviation (x±s), and the Student t -test was used as the statistical method. Results: SGK2 mRNA expression was up-regulated in all 20 HCC samples than that of the expression of matched normal liver tissues. SGK2 protein levels were significantly higher in Huh-7 and SMMC-7721 than normal human liver cell lines (P < 0.01). The downregulation of SGK2 expression in human HCC cell lines (SMMC-7721 and Huh-7) had inhibited the expression of unphosphorylated GSK-3 β. In addition, the downregulation of SGK2 expression in HCC cell lines had decreased the dephosphorylation of β - catenin to prevent degradation of the β - catenin proteasome. Conclusion: SGK2 is overexpressed in HCC and mediates GSK-3β/β- catenin signaling in HCC cells.

目的:探讨多烯磷脂酰胆碱注射液联合注射用丁二磺酸腺苷蛋氨酸治疗胆汁淤积性黄疸患者的疗效.方法:选取胆汁淤积性黄疸患者62例,随机数字表法分为观察组与对照组.对照组予以注射用丁二磺酸腺苷蛋氨酸治疗,观察组在此基础上予以多烯磷脂酰胆碱注射液.统计两组治疗总有效率、不良反应发生率,并对比两组治疗前后肝功能指标水平.结果:观察组治疗总有效率高于对照组;观察组治疗后AST、TBil、ALT、DBil水平低于对照组;差异有统计学意义(P＜0.05);两组不良反应发生率比较无统计学差异(P＞0.05).结论:对胆汁淤积性黄疸患者联合采用注射用丁二磺酸腺苷蛋氨酸、多烯磷脂酰胆碱注射液治疗,可显著改善患者肝功能,提高治疗效果,且安全性高,值得临床推广应用.