HBsAg

Chronic hepatitis B virus (HBV) infection remains a clinical challenge despite the use of nucleoside analogues and interferon-alpha. Peroxisome proliferator-activated receptors (PPARs), which are involved in glucose and lipid metabolism, immune reactions, and inflammation, were studied for their potential role in suppressing HBV replication. In vitro experiments using HepG2 cells transfected with the HBV genome demonstrated that while the PPARalpha ligand bezafibrate had no effect on HBV replication, the PPARgamma ligand rosiglitazone significantly reduced HBV DNA, hepatitis B surface antigen (HBsAg), and hepatitis B e antigen (HBeAg) in the culture supernatant. Southern blot analysis confirmed that rosiglitazone inhibited the replicative intermediates of HBV. The suppressive effect of rosiglitazone was blocked by GW9662, a PPARgamma antagonist. Additionally, rosiglitazone showed a synergistic effect with lamivudine or interferon-alpha-2b in inhibiting HBV replication. This study suggests that rosiglitazone, in combination with nucleoside analogues or interferon, could be a promising therapeutic strategy for chronic HBV infection.