Flavone improves liver damage in nicotine-exposed rats via the Nrf2/HO-1 pathway
Nora A. Elsayed , Fatma SM Moawed , Esraa SA Ahmed , Ahmed Hammad , Omayma AR Abo-Zaid
Asian Pacific Journal of Tropical Biomedicine ›› 2024, Vol. 14 ›› Issue (8) : 341 -349.
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-α, and NF-κB) 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.
Flavone / Nicotine / Liver / Nrf2 / HO-1 / NF-κB
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