Atraric acid alleviates high-fat diet-induced renal injury, lipid accumulation, and fibrosis in mice by regulating oxidative stress and inflammation through AMPK-dependent Nrf2 and NF-κB signaling pathways - 04/02/26
, Tianyue Guan a, b, 1 , Jun Wang a, b , Shasha Zhang a, b , Yusa Li b , Jing Xia b , Panpan Zhao a , Lei Wang c, ⁎ Abstract |
This study explores the protective effects of Atraric Acid (AA) against chronic kidney disease (CKD) induced by a high-fat diet (HFD) and its underlying mechanisms. In vivo HFD-induced CKD mouse models and in vitro OA/PA-stimulated HK2 cells were treated with AA. AA improved kidney morphology, reduced fibrosis, lipid accumulation, and body weight. It also decreased serum TC, TG, HDL-C, Scr, BUN, and Cys-C levels, indicating improved renal function. AA alleviated oxidative stress, ROS accumulation, and inflammation, as confirmed by DHE staining, oxidative stress markers, and pro-inflammatory cytokine levels. Western blotting showed that AA activated Nrf2 and suppressed NF-κB signaling. AMPK inhibition experiments demonstrated that AA regulated Nrf2 and NF-κB via AMPKα phosphorylation. In conclusion, AA mitigates HFD-induced CKD by targeting AMPKα to regulate oxidative stress and inflammation.
Le texte complet de cet article est disponible en PDF.Graphical Abstract |
Highlight |
• | AA alleviates high-fat-induced renal injury, lipid accumulation and fibrosis. |
• | AA mitigates oxidative stress, ROS accumulation and inflammation. |
• | AA attenuates NF-κB mediated inflammation via AMPK activation. |
• | AA alleviates NRF2-mediated oxidative stress via AMPK activation. |
Keywords : Atraric Acid, High-fat diet, Chronic kidney disease, AMPK, Nrf2, NF-κB
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Vol 195
Article 119039- février 2026 Retour au numéro
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