Methane saline suppresses ferroptosis via the Nrf2/HO-1 signaling pathway to ameliorate intestinal ischemia-reperfusion injury.

IF 5.2 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Redox Report Pub Date : 2024-12-01 Epub Date: 2024-07-18 DOI:10.1080/13510002.2024.2373657
Qingrui Fan, Hulin Chang, Lifei Tian, Bobo Zheng, Ruiting Liu, Zeyu Li
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引用次数: 0

Abstract

Objectives: Intestinal ischemia-reperfusion (I/R) injury is a multifactorial and complex clinical pathophysiological process. Current research indicates that the pathogenesis of intestinal I/R injury involves various mechanisms, including ferroptosis. Methane saline (MS) has been demonstrated to primarily exert anti-inflammatory and antioxidant effects in I/R injury. In this study, we mainly investigated the effect of MS on ferroptosis in intestinal I/R injury and determined its potential mechanism.

Methods: In vivo and in vitro intestinal I/R injury models were established to validate the relationship between ferroptosis and intestinal I/R injury. MS treatment was applied to assess its impact on intestinal epithelial cell damage, intestinal barrier disruption, and ferroptosis.

Results: MS treatment led to a reduction in I/R-induced intestinal epithelial cell damage and intestinal barrier disruption. Moreover, similar to treatment with ferroptosis inhibitors, MS treatment reduced ferroptosis in I/R, as indicated by a decrease in the levels of intracellular pro-ferroptosis factors, an increase in the levels of anti-ferroptosis factors, and alleviation of mitochondrial damage. Additionally, the expression of Nrf2/HO-1 was significantly increased after MS treatment. However, the intestinal protective and ferroptosis inhibitory effects of MS were diminished after the use of M385 to inhibit Nrf2 in mice or si-Nrf2 in Caco-2 cells.

Discussion: We proved that intestinal I/R injury was mitigated by MS and that the underlying mechanism involved modulating the Nrf2/HO-1 signaling pathway to decrease ferroptosis. MS could be a promising treatment for intestinal I/R injury.

甲烷生理盐水通过Nrf2/HO-1信号通路抑制铁突变,从而改善肠道缺血再灌注损伤。
目的:肠缺血再灌注(I/R)损伤是一种多因素、复杂的临床病理生理学过程。目前的研究表明,肠缺血再灌注损伤的发病机制涉及多种机制,包括铁变态反应。甲烷生理盐水(MS)已被证实在 I/R 损伤中主要发挥抗炎和抗氧化作用。本研究主要探讨了 MS 对肠 I/R 损伤中铁细胞凋亡的影响,并确定了其潜在机制:方法:建立体内和体外肠道 I/R 损伤模型,验证铁蛋白沉积与肠道 I/R 损伤之间的关系。方法:建立体内和体外肠道 I/R 损伤模型,验证铁蛋白沉积与肠道 I/R 损伤之间的关系;应用 MS 治疗,评估其对肠道上皮细胞损伤、肠道屏障破坏和铁蛋白沉积的影响:结果:MS治疗可减少I/R引起的肠上皮细胞损伤和肠屏障破坏。此外,与使用铁蛋白沉积抑制剂类似,MS治疗也能减少I/R中的铁蛋白沉积,表现为细胞内促铁蛋白沉积因子水平的降低、抗铁蛋白沉积因子水平的升高以及线粒体损伤的减轻。此外,MS治疗后Nrf2/HO-1的表达明显增加。然而,在使用M385抑制小鼠Nrf2或在Caco-2细胞中使用si-Nrf2后,MS的肠道保护和铁突变抑制作用减弱:讨论:我们证明了MS可减轻肠道I/R损伤,其基本机制涉及调节Nrf2/HO-1信号通路以减少铁卟啉沉积。MS可能是一种治疗肠道I/R损伤的有效方法。
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
Redox Report
Redox Report 生物-生化与分子生物学
CiteScore
6.10
自引率
0.00%
发文量
28
审稿时长
>12 weeks
期刊介绍: Redox Report is a multidisciplinary peer-reviewed open access journal focusing on the role of free radicals, oxidative stress, activated oxygen, perioxidative and redox processes, primarily in the human environment and human pathology. Relevant papers on the animal and plant environment, biology and pathology will also be included. While emphasis is placed upon methodological and intellectual advances underpinned by new data, the journal offers scope for review, hypotheses, critiques and other forms of discussion.
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