乙型肝炎病毒抑制载脂蛋白 C3 的体内和体外合成及分泌。
Hepatitis B virus inhibits the in vivo and in vitro synthesis and secretion of apolipoprotein C3.
机构信息
Department of Clinical Laboratory, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, People's Republic of China.
Department of Clinical Laboratory, Shanghai Gongli Hospital, the Second Military Medical University, Pudong New Area, Shanghai, 200135, China.
出版信息
Lipids Health Dis. 2017 Nov 13;16(1):213. doi: 10.1186/s12944-017-0607-2.
BACKGROUND
Hepatitis B virus (HBV) infection in the body can damage liver cells and cause disorders in blood lipid metabolism. Apolipoprotein C3 (ApoC3) plays an important role in the regulation of lipid metabolism, but no study on the HBV regulation of ApoC3 has been reported. This purpose of this study was to investigate the effect of HBV on ApoC3 expression and its regulatory mechanism.
METHODS
The expression levels of ApoC3 mRNA and protein in the human hepatoma cell lines HepG2 and HepG2.2.15 were determined using real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blot. The HepG2 cells were co-transfected with the ApoC3 gene promoter and either HBV-infected clone pHBV1.3 or its individual genes. The changes in luciferase activity were assayed. The expression levels of ApoC3 mRNA and protein were determined using RT-qPCR and Western blot. The content of ApoC3 in the supernatant of the cultured cells was determined using an enzyme-linked immunosorbent assay (ELISA). The sera were collected from 149 patients with HBV infection and 102 healthy subjects at physical examination as the normal controls. The serological levels of ApoC3 in the HBV group and the normal control group were determined using ELISA. The contents of serum triglyceride (TG) and very-low-density lipoprotein (VLDL) in the HBV patients and the normal control were determined using an automatic biochemical analyser.
RESULTS
The expression levels of ApoC3 mRNA and protein were lower in the HepG2.2.15 cells than in the HepG2 cells. pHBV1.3 and its X gene could inhibit the activity of the ApoC3 promoter and its mRNA and protein expression. The serum levels of ApoC3, VLDL and TG were 65.39 ± 7.48 μg/ml, 1.24 ± 0.49 mmol/L, and 0.46 ± 0.10 mmol/L in the HBV patients and 41.02 ± 6.88 μg/ml, 0.76 ± 0.21 mmol/L, 0.29 ± 0.05 mmol/L in the normal controls, respectively, statistical analysis revealed significantly lower serum levels of ApoC3, VLDL and TG in HBV patients than in the normal controls (P < 0.05).
CONCLUSION
HBV can inhibit the in vivo and in vitro synthesis and secretion of ApoC3.
背景
乙型肝炎病毒（HBV）感染体内可损害肝细胞，导致血脂代谢紊乱。载脂蛋白 C3（ApoC3）在脂质代谢调节中发挥重要作用，但尚未有关于 HBV 对 ApoC3 调节的研究报道。本研究旨在探讨 HBV 对 ApoC3 表达的影响及其调控机制。
方法
采用实时定量逆转录聚合酶链反应（RT-qPCR）和 Western blot 检测人肝癌细胞系 HepG2 和 HepG2.2.15 中 ApoC3 mRNA 和蛋白的表达水平。将 ApoC3 基因启动子与 HBV 感染克隆 pHBV1.3 或其单个基因共转染 HepG2 细胞，检测荧光素酶活性的变化。采用 RT-qPCR 和 Western blot 检测 ApoC3 mRNA 和蛋白的表达水平。采用酶联免疫吸附试验（ELISA）检测培养细胞上清液中 ApoC3 的含量。收集 149 例 HBV 感染患者和 102 例健康体检者血清作为正常对照，采用 ELISA 法检测 HBV 组和正常对照组 ApoC3 的血清水平。采用全自动生化分析仪检测 HBV 患者和正常对照组血清三酰甘油（TG）和极低密度脂蛋白（VLDL）含量。
结果
HepG2.2.15 细胞中 ApoC3 mRNA 和蛋白的表达水平低于 HepG2 细胞。pHBV1.3 及其 X 基因可抑制 ApoC3 启动子及其 mRNA 和蛋白的表达。HBV 患者血清 ApoC3、VLDL 和 TG 水平分别为 65.39±7.48μg/ml、1.24±0.49mmol/L 和 0.46±0.10mmol/L，正常对照组分别为 41.02±6.88μg/ml、0.76±0.21mmol/L 和 0.29±0.05mmol/L，HBV 患者血清 ApoC3、VLDL 和 TG 水平明显低于正常对照组（P<0.05）。
结论
HBV 可抑制体内外 ApoC3 的合成和分泌。
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