Effect of ganoderic acid on diethylnitrosamine-induced liver cancer in mice

Abstract

Purpose: To investigate the hepatoprotective role of ganoderic acid A (GAA) on liver cancer induced by diethylnitrosamine (DEN) via Nrf-2/HO-1/NF-κB signal pathway in mice. Methods: Sixty male C57BL/6J mice were randomly divided into 4 groups: (1) control group, (2) DEN (25 mg/kg) group, (3) GAA (20 mg/kg) + DEN group, (4) GAA (40 mg/kg) + DEN group. The protective effect of GAA on liver was evaluated by determining malondialdehyde (MDA), superoxide dismutase (SOD), inflammatory cytokines including interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and the expression of heme oxygenase-1 (HO-1), nuclear factor erythroid- 2-related factor-2 (Nrf-2), IκBα, p-IκBα, p65, p-p65, glyceraldehyde-3-phosphate dehydrogenase (GAPDH) in serum. Results: The results demonstrate that GAA treatment significantly suppressed the generation of MDA, proinflammatory cytokines, and restored the activity of SOD in the serum of DEN-induced liver cancer in mice. Western blots analysis revealed that GAA significantly restored Nrf-2/HO-1/NF-κB signal pathwayrelated protein levels in DEN-induced mice liver cancer model. Conclusion: This research reveals the anticancer activity of GAA in liver tissue, and suggests that GAA counters DEN-induced liver cancer through Nrf-2/HO-1/NF-κB signal pathway.