Lycopene-Loaded Bilosomes Ameliorate High-Fat Diet-Induced Chronic Nephritis in Mice through the TLR4/MyD88 Inflammatory Pathway

番茄红素 尿酸 内分泌学 内科学 TLR4型 炎症 药理学 肌酐 医学 化学 抗氧化剂 生物化学
作者
Chang Liu,Yu Liu,Ciwan Wang,Yahui Guo,Yuliang Cheng,He Qian,Yong Zhao
出处
期刊:Foods [MDPI AG]
卷期号:11 (19): 3042-3042 被引量:9
标识
DOI:10.3390/foods11193042
摘要

Chronic kidney disease caused by a high-fat diet (HFD)-induced metabolic syndrome has received widespread attention. Lycopene has a wide range of biological activities and can improve a variety of chronic diseases through anti-inflammatory effects. In this study, HFD-fed mice were used as a metabolic syndrome model to evaluate the protective effect of lycopene in a sustained-release vehicle (bilosomes) in the small intestine against renal injury and to determine whether the TLR4/MyD88 pathway and related metabolic pathways are involved in this process. The results showed that lycopene bilosomes alleviated HFD-induced kidney damage, as evidenced by lower serum urea nitrogen, creatinine, and uric acid levels. Histopathology studies showed that lycopene bilosomes attenuated HFD-induced tubular cell and glomerular injury. In addition, Elisa, RT-PCR, and Western blotting results showed that lycopene bilosomes also reduced the expression of inflammatory factors such as TLR4, MyD88, NF-kB, TNF-a, and IL-6 in mouse kidneys. The mechanism was to attenuate renal inflammatory response by inhibiting the TLR4/MyD88 inflammatory pathway. These findings suggested that lycopene can alleviate nephritis and metabolic disorders caused by HFD, inhibiting the TLR4/MyD88 inflammatory pathway and its downstream pro-inflammatory cytokines and further regulating the vitamin K metabolism, beta-alanine metabolism, and glutathione metabolism pathways to relieve chronic nephritis.
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