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岩藻黄质通过 PI3K/AKT 信号通路介导 Nrf2 对玉米赤霉烯酮诱导的肝损伤的保护作用。

Protective Effect of Fucoxanthin on Zearalenone-Induced Hepatic Damage through Nrf2 Mediated by PI3K/AKT Signaling.

机构信息

Department of Biological Sciences, College of Science, King Faisal University, Al-Ahsa 31982, Saudi Arabia.

Center of Biotechnology of Borj-Cedria, Laboratory of Aromatic and Medicinal Plants, Technopole of Borj-Cedria, Hammam-Lif 2050, Tunisia.

出版信息

Mar Drugs. 2023 Jul 3;21(7):391. doi: 10.3390/md21070391.

DOI:10.3390/md21070391
PMID:37504922
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10381773/
Abstract

Hepatotoxic contaminants such as zearalenone (ZEA) are widely present in foods. Marine algae have a wide range of potential applications in pharmaceuticals, cosmetics, and food products. Research is ongoing to develop treatments and products based on the compounds found in algae. Fucoxanthin (FXN) is a brown-algae-derived dietary compound that is reported to prevent hepatotoxicity caused by ZEA. This compound has multiple biological functions, including anti-diabetic, anti-obesity, anti-microbial, and anti-cancer properties. Furthermore, FXN is a powerful antioxidant. In this study, we examined the effects of FXN on ZEA-induced stress and inflammation in HepG2 cells. MTT assays, ROS generation assays, Western blots, and apoptosis analysis were used to evaluate the effects of FXN on ZEA-induced HepG2 cell inflammation. Pre-incubation with FXN reduced the cytotoxicity of ZEA toward HepG2 cells. FXN inhibited the ZEA-induced production of pro-inflammatory cytokines, including IL-1 β, IL-6, and TNF-α. Moreover, FXN increased HO-1 expression in HepG2 by activating the PI3K/AKT/NRF2 signaling pathway. In conclusion, FXN inhibits ZEA-induced inflammation and oxidative stress in hepatocytes by targeting Nrf2 via activating PI3K/AKT signaling.

摘要

肝毒性污染物,如玉米赤霉烯酮(ZEA),广泛存在于食品中。海洋藻类在药物、化妆品和食品产品方面有广泛的潜在应用。目前正在研究基于藻类中发现的化合物开发治疗方法和产品。岩藻黄素(FXN)是一种源自褐藻的膳食化合物,据报道可预防 ZEA 引起的肝毒性。这种化合物具有多种生物学功能,包括抗糖尿病、抗肥胖、抗微生物和抗癌特性。此外,FXN 是一种强大的抗氧化剂。在这项研究中,我们研究了 FXN 对 HepG2 细胞中 ZEA 诱导的应激和炎症的影响。MTT 测定法、ROS 生成测定法、Western blot 和细胞凋亡分析用于评估 FXN 对 ZEA 诱导的 HepG2 细胞炎症的影响。FXN 的预孵育降低了 ZEA 对 HepG2 细胞的细胞毒性。FXN 抑制了 ZEA 诱导的促炎细胞因子的产生,包括 IL-1β、IL-6 和 TNF-α。此外,FXN 通过激活 PI3K/AKT/NRF2 信号通路增加了 HepG2 中的 HO-1 表达。总之,FXN 通过激活 PI3K/AKT 信号靶向 Nrf2 抑制 ZEA 诱导的肝细胞炎症和氧化应激。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c002/10381773/54fd3c234319/marinedrugs-21-00391-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c002/10381773/f5e60f77830c/marinedrugs-21-00391-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c002/10381773/1e464c6a098d/marinedrugs-21-00391-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c002/10381773/f306594d1b87/marinedrugs-21-00391-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c002/10381773/dfd8388731cd/marinedrugs-21-00391-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c002/10381773/54fd3c234319/marinedrugs-21-00391-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c002/10381773/f5e60f77830c/marinedrugs-21-00391-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c002/10381773/1e464c6a098d/marinedrugs-21-00391-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c002/10381773/f306594d1b87/marinedrugs-21-00391-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c002/10381773/dfd8388731cd/marinedrugs-21-00391-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c002/10381773/54fd3c234319/marinedrugs-21-00391-g005.jpg

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