Liver cancer-related gene CYP2E1 expression in HBV transgenic mice with acute liver injury

Abstract

The objective of this research was to study the CYP2E1 gene expression in carbon tetrachloride (CCl4)-induced acute liver injury in hepatitis B virus (HBV) transgenic mice. Twenty-four HBV(-) and 24 HBV(+) transgenic mice aged 8 to 10 weeks were selected for the present study. Intraperitoneal injection of 1.0 μL/g of CCl4 (1:4 dissolved in olive oil) to mice was performed to induce acute liver injury model. Eight normal clean-grade C57BL/6 mice were taken as the control group. The control group received saline intraperitoneally. The mice in each group were killed 3, 6, 12, 24, 48, and 72 h after injection. The liver tissue samples of mice were collected. The liver histological changes at different time points in each group were observed under light microscope. The quantitative PCR methods were utilized to measure the relative mRNA levels of CYP2E1 gene in liver tissues. Immunohistochemistry and Western blot techniques were used to observe tissue expression levels of CYP2E1 in each group. Compared with that of the control group, mRNA and protein expression levels of CYP2E1 significantly increased both in the HBV(-) group and in the HBV(+) group after the CCl4 induced the acute liver injury, and it reached the peak at 72h after the CCl4 injection. Compared with the HBV(-) group, the mice in the HBV(+) group had severe liver damage and significantly increased CYP2E1 gene and protein expression levels. In the CCl4-induced acute liver injury of HBV transgenic mice, the CYP2E1 gene expression significantly increased. The results provided evidence for the HBV-induced liver damage and liver cancer pathogenesis.