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

Abstract

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.

A Flavonoid Glycoside Compound from Siraitia grosvenorii with Anti-Inflammatory and Hepatoprotective Effects In Vitro

“…The inflammatory cytokines IL-1β, IL-6, and IL-10 have an important role in the inflammatory process, in which expression levels and action mechanisms contribute to the comprehension of disease pathogenesis and therapeutic approaches. The TLR4/NF-κB/MyD88 pathway has been recognized as a central link in the pathogenic process of systemic inflammation [29]. In the present study, on the one hand, TLR4/MyD88 activation has been found to be notably upregulated in LPSinduced MH-S cells, leading to increased expression of pro-inflammatory cytokines and related chemokines, including TNF-a, IL-1β, IL-6, and IL-10.…”

Resveratrol Improves Hyperuricemia and Ameliorates Renal Injury by Modulating the Gut Microbiota

“…Therefore, controlling the level of serum UA within the normal range will help alleviate renal injury. Studies have shown that HFD feeding can lead to HUA and chronic kidney injury in mice, the specific pathological manifestations of which are glomerular atrophy, the proliferation of mesangial cells and mesangial matrix, unclear renal tubule structure, fibrosis, and chronic inflammation [23,24]. In this study, HFD-fed mice treated with RES had less glomerular atrophy and clearer renal tubule structures, as observed by HE staining, while the areas of Masson and PAS-positive staining were reduced, indicating decreased renal fibrosis and mesangial matrix proliferation, respectively.…”

Bilosomes and Biloparticles for the Delivery of Lipophilic Drugs: A Preliminary Study

“…These results indicate that the bilosystem (either bilosome or biloparticle) is able to increase the solubility and to control the release of the incorporated drug. Furthermore, these data revealed the significant dominance of the bilosystem to enhance the intestinal passage of budesonide, possibly due to the ability of these nanocarriers to improve the intestinal permeability of the encapsulated drugs [42][43][44][45][46][47][48][49][50][51][52][53][54][55][56].…”