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含有促消退介质的鱼油可增强抗氧化系统并减轻脂多糖诱导的人支气管上皮细胞炎症。

Fish Oil Containing Pro-Resolving Mediators Enhances the Antioxidant System and Ameliorates LPS-Induced Inflammation in Human Bronchial Epithelial Cells.

作者信息

Distefano Alfio, Orlando Laura, Giallongo Sebastiano, Tropea Emanuela, Spampinato Mariarita, Santisi Annalisa, Longhitano Lucia, Parisi Giuseppe, Leonardi Salvatore, Russo Arcangelo, Caruso Massimo, Di Rosa Michelino, Tibullo Daniele, Salamone Maurizio, Li Volti Giovanni, Barbagallo Ignazio Alberto

机构信息

Department of Biomedical and Biotechnological Sciences, University of Catania, 95123 Catania, Italy.

Department of Medical, Surgical Sciences and Advanced Technologies "G.F. Ingrassia", University of Catania, 95123 Catania, Italy.

出版信息

Pharmaceuticals (Basel). 2024 Aug 14;17(8):1066. doi: 10.3390/ph17081066.

DOI:10.3390/ph17081066
PMID:39204170
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11360764/
Abstract

Fish oil, renowned for its high content of omega-3 fatty acids, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), has gained considerable attention for its potential health benefits. EPA and DHA exhibit anti-inflammatory effects by promoting the production of specialized pro-resolving mediators (SPMs), such as resolvins and protectins. Fish oil has been studied for its potential to reduce bronchial inflammation, a key feature of respiratory conditions like asthma and COPD. This study investigates the cellular mechanisms of fish oil in an in vitro model of lung inflammation using lipopolysaccharide (LPS) on a healthy human bronchial epithelium cell line. LPS exposure for 24 h reduced cell viability, elevated reactive oxygen species (ROS), depleted glutathione (GSH), and induced mitochondrial depolarization, indicating oxidative stress and inflammation. Fish oil administration significantly mitigated ROS production, prevented GSH depletion, and reduced mitochondrial depolarization. This was associated with the upregulation of the endogenous antioxidant system, evidenced by restored GSH levels and the increased gene expression of glutathione peroxidase (GPX), catalase (CAT), superoxide dismutase 1 (SOD1), and superoxide dismutase 2 (SOD2). Fish oil also suppressed IL-6 and IL-1β expression and increased anti-inflammatory cytokine IL-10 expression. Furthermore, fish oil upregulated the expression of pro-resolving mediator receptors, suggesting a role in inflammation resolution. These findings highlight the potential of fish oil supplementation as a preventive measure against pulmonary diseases characterized by unresolved inflammation such as lung inflammation.

摘要

鱼油以其富含ω-3脂肪酸,特别是二十碳五烯酸(EPA)和二十二碳六烯酸(DHA)而闻名,因其潜在的健康益处而备受关注。EPA和DHA通过促进特异性促消退介质(SPM)如消退素和保护素的产生而发挥抗炎作用。鱼油降低支气管炎症的潜力已得到研究,支气管炎症是哮喘和慢性阻塞性肺疾病(COPD)等呼吸系统疾病的一个关键特征。本研究使用脂多糖(LPS)在健康人支气管上皮细胞系上建立肺部炎症体外模型,研究鱼油的细胞机制。暴露于LPS 24小时会降低细胞活力、升高活性氧(ROS)、消耗谷胱甘肽(GSH)并诱导线粒体去极化,表明存在氧化应激和炎症。给予鱼油可显著减轻ROS的产生、防止GSH消耗并减少线粒体去极化。这与内源性抗氧化系统的上调有关,表现为GSH水平恢复以及谷胱甘肽过氧化物酶(GPX)、过氧化氢酶(CAT)、超氧化物歧化酶1(SOD1)和超氧化物歧化酶2(SOD2)的基因表达增加。鱼油还抑制白细胞介素-6(IL-6)和白细胞介素-1β(IL-1β)的表达,并增加抗炎细胞因子白细胞介素-10(IL-10)的表达。此外,鱼油上调了促消退介质受体的表达,表明其在炎症消退中发挥作用。这些发现凸显了补充鱼油作为预防以未解决的炎症为特征的肺部疾病如肺部炎症的潜在作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/260b/11360764/72e2dbe1cb13/pharmaceuticals-17-01066-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/260b/11360764/16b66e898bec/pharmaceuticals-17-01066-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/260b/11360764/2f6c7a71c507/pharmaceuticals-17-01066-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/260b/11360764/9d3217477ee7/pharmaceuticals-17-01066-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/260b/11360764/6fa275368776/pharmaceuticals-17-01066-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/260b/11360764/72e2dbe1cb13/pharmaceuticals-17-01066-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/260b/11360764/16b66e898bec/pharmaceuticals-17-01066-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/260b/11360764/2f6c7a71c507/pharmaceuticals-17-01066-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/260b/11360764/9d3217477ee7/pharmaceuticals-17-01066-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/260b/11360764/72e2dbe1cb13/pharmaceuticals-17-01066-g005.jpg

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