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岩藻黄质通过调节 AMPK/Nrf2/TLR4 信号通路来减轻游离脂肪酸诱导的非酒精性脂肪性肝病中的脂质代谢/氧化应激/炎症。

Fucoxanthin Attenuates Free Fatty Acid-Induced Nonalcoholic Fatty Liver Disease by Regulating Lipid Metabolism/Oxidative Stress/Inflammation via the AMPK/Nrf2/TLR4 Signaling Pathway.

机构信息

Zhejiang Provincial Engineering Technology Research Center of Marine Biomedical Products, School of Food and Pharmacy, Zhejiang Ocean University, Zhoushan 316022, China.

出版信息

Mar Drugs. 2022 Mar 25;20(4):225. doi: 10.3390/md20040225.

DOI:10.3390/md20040225
PMID:35447899
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9027317/
Abstract

Fucoxanthin, a xanthophyll carotenoid abundant in brown algae, is reported to have several biological functions, such as antioxidant, anti-inflammatory, and anti-tumor activities, in mice. We investigated the effects and mechanisms of fucoxanthin in the mixture oleate/palmitate = 2/1(FFA)-induced nonalcoholic fatty liver disease (NAFLD) cell model in this study. The results showed that the content of superoxide dismutase in the FFA group was 9.8 ± 1.0 U/mgprot, while that in the fucoxanthin high-dose (H-Fx) group (2 μg/mL) increased to 22.9 ± 0.6 U/mgprot. The content of interleukin-1β in the FFA group was 89.3 ± 3.6 ng/mL, while that in the H-Fx group was reduced to 53.8 ± 2.8 ng/mL. The above results indicate that fucoxanthin could alleviate the FFA-induced oxidative stress and inflammatory levels in the liver cells. Oil red-O staining revealed visible protrusions and a significant decrease in the number of lipid droplets in the cytoplasm of cells in the fucoxanthin group. These findings on the mechanisms of action suggest that fucoxanthin can repair FFA-induced NAFLD via the adenosine monophosphate-activated protein kinase (AMPK) signaling pathway and nuclear factor erythroid-2-related factor 2-mediated (Nrf2) signaling pathway, as well as by downregulating the expression of the Toll-like receptor 4-mediated (TLR4) signaling pathway. Fucoxanthin exhibited alleviating effects in the FFA-induced NAFLD model and could be explored as a potential anti-NAFLD substance.

摘要

岩藻黄质是一种在褐藻中含量丰富的叶黄素类胡萝卜素,据报道,它在小鼠体内具有多种生物学功能,如抗氧化、抗炎和抗肿瘤活性。本研究旨在探讨岩藻黄质在油酸/棕榈酸(FFA)混合物诱导的非酒精性脂肪性肝病(NAFLD)细胞模型中的作用及其机制。结果表明,FFA 组中超氧化物歧化酶的含量为 9.8±1.0 U/mgprot,而岩藻黄质高剂量(H-Fx)组(2μg/mL)增加到 22.9±0.6 U/mgprot。FFA 组白细胞介素-1β的含量为 89.3±3.6ng/mL,而 H-Fx 组降低至 53.8±2.8ng/mL。上述结果表明,岩藻黄质可以减轻 FFA 诱导的肝细胞氧化应激和炎症水平。油红-O 染色显示,岩藻黄质组细胞的细胞质中可见明显的突起和脂滴数量显著减少。这些作用机制的研究结果表明,岩藻黄质可以通过腺苷单磷酸激活蛋白激酶(AMPK)信号通路和核因子红细胞 2 相关因子 2 介导的(Nrf2)信号通路修复 FFA 诱导的 NAFLD,同时下调 Toll 样受体 4 介导的(TLR4)信号通路的表达。岩藻黄质在 FFA 诱导的 NAFLD 模型中表现出缓解作用,可作为一种潜在的抗 NAFLD 物质进行探索。

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