Flavone improves liver damage in nicotine-exposed rats via the Nrf2/HO-1 pathway

Objective: To assess the hepatoprotective effects of flavone on nicotine-induced liver damage. Methods: Thirty-six rats were allocated into six groups: the control group, the nicotine group, the flavone alone groups (10 and 25 mg/ kg/body weight), and the nicotine groups treated with flavone (10 and 25 mg/kg/body weight). Liver function, oxidative stress, Nrf2 pathway (HO-1, Nrf2, and Keap-1), and inflammatory markers (IL-17, TNF-alpha, and NF-kappa B) were evaluated. Additionally, a histopathological examination of liver tissues was performed. Results: Nicotine increased liver damage, inflammation, and oxidative stress. However, flavone suppressed nicotine-induced liver enzymes, oxidative stress, and inflammation, as manifested by increased antioxidants and decreased malondialdehyde level, liver enzymatic activities, and inflammatory markers. Flavone (10 and 25 mg/kg/body weight) also reduced the level of Keap-1 and increased HO-1 and Nrf2 levels in the liver of nicotine-exposed rats. Conclusions: Flavone has hepatoprotective properties and may slow the progression of liver injury by reducing oxidative stress, liver enzymes, and inflammation possibly via the Nrf2 pathway.