HBx inhibits HMGB1 expression and active oxygen production in LO2 cells through the NF-κB signaling pathway.

Hepatitis B virus (HBV) infection is one of major causes of various kinds of liver diseases. Among the four open reading frames (ORFs) of the HBV genome, the X region of HBV encodes HBx protein, which plays an important regulatory role in HBV infection. NF-κB and high-mobility group protein box1 (HMGB1) are potentially able to enhance the scavenging activity of host cells against foreign microorganisms. The present study focuses on the effect of HBx on the expression of HMGB1 in vitro. First, the lentiviral vector was used to induce the overexpression of HBx protein in LO2 cells (a normal hepatocyte cell line). Then, NF-κB activity, HMGB1 expression and the production of ROS were detected by Western blot and DCFH-DA (ROS detector) staining. Afterward, rotenone and LPS, which are activors of ROS and NF-κB, respectively, were used to stimulate HBx-overexpressing cells. Then, the expression differentiation of HMGB1 and ROS or the activity alternation of NF-κB was detected again. HBx inhibited the activity of NF-κB, inhibited the expression of HMGB1 and inhibited the production of ROS. The stimulation study with retenone or LPS suggested that there were mutual regulations between NF-κB and HMGB1. HBx inhibits the expression of HMGB1 and the generation of ROS via the NF-κB signaling pathway.