期刊
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
卷 71, 期 48, 页码 18769-18779出版社
AMER CHEMICAL SOC
DOI: 10.1021/acs.jafc.3c05735
关键词
nuciferine; obesity-inducednephrotoxicity; hypolipidemic; oxidative stress; inflammation
This study investigated the protective effects of nuciferine on kidney damage caused by high-fat diets and its underlying mechanisms. The results showed that nuciferine could alleviate chronic renal dysfunction, delay renal fibrosis progression, and prevent podocyte apoptosis. It achieved these effects by reducing renal lipid accumulation, suppressing inflammation and oxidative stress, and regulating key protein factors.
High-fat diets (HFD) could cause obesity, trigger lipid accumulation, and induce oxidative stress and inflammation, leading to kidney damage. This study aimed to elucidate the protective effects of nuciferine on HFD-caused nephrotoxicity and explore the underlying mechanisms in Kunming mice and palmitic acid-exposed HK-2 cells. In obese mice, nuciferine notably alleviated HFD-induced chronic renal dysfunction and delayed renal fibrosis progression and podocyte apoptosis, as evidenced by the increased expressions of renal function factors BUN, CRE, and UA and the decreased expressions of key protein factors TGF-beta 1, p-Samd3, Wnt-1, and beta-catenin. Nuciferine also effectively attenuated HFD-induced renal lipid accumulation via the AMPK-mediated regulation of FAS and HSL expressions and suppressed inflammation and oxidative stress via the AMPK-mediated Nrf-2/HO-1 and TLR4/MyD88/NF-kappa B pathways. In addition, consistent with the results of animal experiments, nuciferine remarkably reversed cell damage and attenuated lipid accumulation, inflammation, and oxidative stress in palmitic acid-exposed HK-2 cells through the AMPK-mediated signaling pathway. Therefore, nuciferine could be a new food-derived protective agent to offset obesity and correlative kidney damage.
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