Abstract
BackgroundHepatitis 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.MethodsThe 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.ResultsThe 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).ConclusionHBV can inhibit the in vivo and in vitro synthesis and secretion of ApoC3.
Highlights
Hepatitis B virus (HBV) infection in the body can damage liver cells and cause disorders in blood lipid metabolism
The serum High-density lipoprotein cholesterol (HDL-C), Low-density lipoprotein cholesterol (LDL-C), Total cholesterol (TC), ApoA1 and ApoB were significantly lower in HBV patients comparing with healthy individuals (p < 0.05), while there was no significant difference in gender, age and Body mass index (BMI) between the two groups (P > 0.05)
The results showed that the expression levels of Apolipoprotein C3 (ApoC3) in HepG2 and HepG2.2.15 cells were 46.15 ± 9.58 μg/ml and 28.02 ± 8.46 μg/ml, respectively, with a statistically significant difference (P < 0.05, Fig. 1c), indicating that HBV can inhibit the expression of ApoC3 in HepG2 cells
Summary
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. Of the C family members, apolipoprotein C3 (ApoC3) is seen at the highest concentration; its gene is located on the long arm q23 region of chromosome 11 and includes 4 exons and 3 introns.
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