Ferroptosis inhibition shields house ear institute-organ of corti 1 cells from free fatty acids-induced inflammatory injuries.

IF 1.2 4区 医学 Q3 OTORHINOLARYNGOLOGY Acta Oto-Laryngologica Pub Date : 2023-05-01 DOI:10.1080/00016489.2023.2202688
Xuemin Chen, Yiding Yu, Ning Yu, Weiwei Guo, Qingqing Jiang, Shiming Yang
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引用次数: 0

Abstract

Background: Free fatty acids (FFAs) could induce inflammatory responses via various pathways. Ferroptosis is characterized by the accumulation of lipid peroxidation products and fatal reactive oxygen species derived from iron accumulation, which may be an upstream event in the inflammatory injuries.

Objectives: To investigate the involvement of ferroptosis during the FFAs-induced pathological hair cell inflammatory injuries and its underlying mechanisms.

Material and methods: We utilized House Ear Institute-Organ of Corti 1 (HEI-OC1) cell line as an in vitro model. The palmitate acid (PA) was utilized as a substitute for FFA, with cotreatment with ferroptosis inducer RSL3 and ferroptosis inhibitor Fer-1. Cell viability, lactase dehydrogenase (LDH) release, the expressions of ferroptosis-related factors such as glutathione peroxidase-4 (GPX4), solute carrier family 7 member 11 (SLC7A11), as well as toll-like receptor 4 (TLR4), ferric ion and reactive oxygen species (ROS), and partial inflammatory cytokines were measured.

Results: PA treatment might induce ferroptosis in HEI-OC1 cells, manifested as decreased cell viability, upregulated LDH release, iron overload, and ROS accumulation. Several inflammatory cytokines including IL-1β, IL-6, IL-1β, IL-6, TNF-α, MCP-1, IL-13, IL-12 p40, CCL5, G-CSF, and GM-CSF were upregulated compared to the Ctr group, while GPX4 and SLC7A11 were downregulated. The expression of TLR4 in the inflammatory pathway was also upregulated. Besides, these changes were further exacerbated by RSL3 cotreatment and abolished by Fer-1 cotreatment.

Conclusions and significance: Ferroptosis inhibition could alleviate the PA-induced inflammatory injuries via inactivation of TLR4 signaling pathway in HEI-OC1 cell line.

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铁下垂抑制保护耳研究所器官的corti 1细胞免受游离脂肪酸诱导的炎症损伤。
背景:游离脂肪酸(FFAs)可通过多种途径诱导炎症反应。铁下垂的特点是脂质过氧化产物和铁积累引起的致命活性氧的积累,这可能是炎症损伤的上游事件。目的:探讨铁下垂在ffas诱导的病理性毛细胞炎症损伤中的作用及其机制。材料与方法:以House Ear Institute-Organ of Corti 1 (HEI-OC1)细胞系为体外模型。采用棕榈酸(PA)代替FFA,与铁下垂诱导剂RSL3和铁下垂抑制剂Fer-1共处理。测定细胞活力、乳酸脱氢酶(LDH)释放、凋亡相关因子如谷胱甘肽过氧化物酶4 (GPX4)、溶质载体家族7成员11 (SLC7A11)、toll样受体4 (TLR4)、铁离子和活性氧(ROS)、部分炎症因子的表达。结果:PA处理可诱导HEI-OC1细胞铁下垂,表现为细胞活力降低、LDH释放上调、铁超载、ROS积累。与Ctr组相比,IL-1β、IL-6、IL-1β、IL-6、TNF-α、MCP-1、IL-13、IL-12 p40、CCL5、G-CSF和GM-CSF等炎症因子上调,GPX4和SLC7A11下调。TLR4在炎症通路中的表达也上调。此外,RSL3共处理进一步加剧了这些变化,而fe -1共处理则消除了这些变化。结论及意义:抑制铁下垂可通过使HEI-OC1细胞株TLR4信号通路失活来减轻pa诱导的炎症损伤。
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来源期刊
Acta Oto-Laryngologica
Acta Oto-Laryngologica 医学-耳鼻喉科学
CiteScore
2.50
自引率
0.00%
发文量
99
审稿时长
3-6 weeks
期刊介绍: Acta Oto-Laryngologica is a truly international journal for translational otolaryngology and head- and neck surgery. The journal presents cutting-edge papers on clinical practice, clinical research and basic sciences. Acta also bridges the gap between clinical and basic research.
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