Objective: To investigate the protective effects of naringin on doxorubicin (DOX)-induced liver injury. Methods: A total of 50 male rats were allocated into five groups: the control group, the DOX group, the DOX groups treated with 50 mg/kg and 100 mg/kg of naringin by gastric lavage for 10 days, as well as the group treated with 100 mg/kg of naringin alone. Liver and serum samples were collected for biochemical, histopathological, and molecular analyses, including liver enzyme activity, oxidative stress markers, inflammation, apoptosis-related proteins, and DNA damage indicators. Results: Naringin attenuated DOX-induced elevation in liver enzyme activity and inflammation markers while enhancing antioxidant activities. Naringin also activated the Nrf2-HO-1 signaling pathway, with the most pronounced effect in the high-dose naringin group. In addition, naringin modulated apoptotic signaling by downregulating the expression of PI3K-AKT and BAX, and upregulating Bcl-2, as well as reduced the level of 8-OHdG. Histopathological evaluation showed that DOX-induced structural liver alterations, such as cellular degeneration and necrosis, were notably attenuated by naringin treatment. Conclusions: Naringin treatment exerts protective effects against DOX-induced liver injury through its antioxidative, anti-inflammatory, and anti-apoptotic effects.
Azman et al. (Tue,) studied this question.
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