NOX4 induces oxidative stress and apoptosis through upregulation of caspases 3 and 9 and downregulation of TIGAR in HCV-infected Huh-7 cells

Aim: The present study was designed to determine the potential role of oxidative stress in the induction of apoptosis in a transient in vitro model of HCV-infected Huh-7 cells. Material & methods: A transient in vitro infectivity model of a Huh-7 cell line was established using serum from HCV genotype 3a patients. Quantitative expression of selected genes was measured using real-time PCR. Results: A test of the apoptotic responses of cells under stressful conditions showed a significant increase in selected oxidative stress and apoptotic markers, along with a significant decrease in expression of antioxidants following inoculation in a time-dependent manner. A significant decrease in TIGAR and a significant increase in p53 expression levels at day 6 suggested the possible role of p53 and TIGAR in the induction of apoptosis and oxidative stimuli in experimental Huh-7/HCV cell lines. Conclusion: Collectively, the findings of the current study suggest a role for p53 and TIGAR in HCV-induced apoptosis in the presence of oxidative stress in a Huh-7 cell line.