Epigallocatechin-3-gallate Alleviates Ethanol-Induced Endothelia Cells Injury Partly through Alteration of NF-κB Translocation and Activation of the Nrf2 Signaling Pathway.

IF 1.7 4区 医学 Q3 PHARMACOLOGY & PHARMACY
Biological & pharmaceutical bulletin Pub Date : 2024-07-05 Epub Date: 2024-06-12 DOI:10.1248/bpb.b23-00773
Jie Xu, Shouzhu Xu, Jiayin Luo, Shihao Zhang, Dongdong Wu, Qifan Yang, Rourou Fang, Chuandao Shi, Qiling Liu, Jing Zhao
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Abstract

Ethanol (alcohol) is a risk factor that contributes to non-communicable diseases. Chronic abuse of ethanol is toxic to both the heart and overall health, and even results in death. Ethanol and its byproduct acetaldehyde can harm the cardiovascular system by impairing mitochondrial function, causing oxidative damage, and reducing contractile proteins. Endothelial cells are essential components of the cardiovascular system, are highly susceptible to ethanol, either through direct or indirect exposure. Thus, protection against endothelial injury is of great importance for persons who chronic abuse of ethanol. In this study, an in vitro model of endothelial injury was created using ethanol. The findings revealed that a concentration of 20.0 mM of ethanol reduced cell viability and Bcl-2 expression, while increasing cell apoptosis, intracellular reactive oxygen species (ROS) levels, mitochondrial depolarization, and the expression of Bax and cleaved-caspase-3 in endothelial cells. Further study showed that ethanol promoted nuclear translocation of nuclear factor kappa B (NF-κB), increased the secretion of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 in the culture medium, and inhibited nuclear factor-erythroid 2-related factor 2 (Nrf2) signaling pathway. The aforementioned findings suggest that ethanol has a harmful impact on endothelial cells. Nevertheless, the application of epigallocatechin-3-gallate (EGCG) to the cells can effectively mitigate the detrimental effects of ethanol on endothelial cells. In conclusion, EGCG alleviates ethanol-induced endothelial injury partly through alteration of NF-κB translocation and activation of the Nrf2 signaling pathway. Therefore, EGCG holds great potential in safeguarding individuals who chronically abuse ethanol from endothelial dysfunction.

表没食子儿茶素-3-没食子酸酯部分通过改变NF-κB转位和激活Nrf2信号通路,减轻乙醇诱导的内皮细胞损伤。
乙醇(酒精)是导致非传染性疾病的一个风险因素。长期滥用乙醇会对心脏和整体健康造成毒害,甚至导致死亡。乙醇及其副产品乙醛会损害线粒体功能、造成氧化损伤和减少收缩蛋白,从而伤害心血管系统。内皮细胞是心血管系统的重要组成部分,极易直接或间接接触乙醇。因此,防止内皮损伤对长期滥用乙醇的人来说非常重要。本研究利用乙醇建立了一个内皮损伤的体外模型。研究结果表明,浓度为 20.0 mM 的乙醇会降低细胞活力和 Bcl-2 的表达,同时增加细胞凋亡、细胞内 ROS 水平、线粒体去极化以及内皮细胞中 Bax 和裂解-caspase-3 的表达。进一步的研究表明,乙醇能促进 NF-κB 的核转位,增加培养液中 TNF-α、IL-1β、IL-6 的分泌,抑制 Nrf2 信号通路。上述研究结果表明,乙醇会对内皮细胞产生有害影响。然而,向细胞中添加表没食子儿茶素-3-棓酸盐(EGCG)可以有效缓解乙醇对内皮细胞的有害影响。总之,EGCG 部分通过改变 NF-κB 转位和激活 Nrf2 信号通路来减轻乙醇诱导的内皮损伤。因此,EGCG 在保护长期滥用乙醇的人免受内皮功能障碍方面具有很大的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
3.50
自引率
5.00%
发文量
247
审稿时长
2 months
期刊介绍: Biological and Pharmaceutical Bulletin (Biol. Pharm. Bull.) began publication in 1978 as the Journal of Pharmacobio-Dynamics. It covers various biological topics in the pharmaceutical and health sciences. A fourth Society journal, the Journal of Health Science, was merged with Biol. Pharm. Bull. in 2012. The main aim of the Society’s journals is to advance the pharmaceutical sciences with research reports, information exchange, and high-quality discussion. The average review time for articles submitted to the journals is around one month for first decision. The complete texts of all of the Society’s journals can be freely accessed through J-STAGE. The Society’s editorial committee hopes that the content of its journals will be useful to your research, and also invites you to submit your own work to the journals.
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