Serum of limb remote ischemic postconditioning inhibits fMLP-triggered activation and reactive oxygen species releasing of rat neutrophils.

IF 5.2 2区生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Redox Report Pub Date : 2021-12-01 DOI:10.1080/13510002.2021.1982515

Gangling Chen, Jiangwei Zhang, Mingyue Sheng, Sanli Zhang, Qi Wu, Lei Liu, Boyang Yu, Junping Kou

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引用次数: 1

Abstract

Objectives: The study explores the protective role of the peripheral serum of limb remote ischemic postconditioning (LRIP) in reducing the reactive oxygen species (ROS) levels and neutrophil activation, which are responsible for the deleterious reperfusion injury.

Methods: LRIP was induced in Sprague-Dawley rats by three cycles of 5 min occlusion /5 min reperfusion on the left hind limb. The blood samples were collected before LRIP or 0 and 1 h after LRIP (named Serum_Sham, Serum_LRIP0, Serum_LRIP1, respectively). The effects of LRIP serum on ROS level and neutrophils activation were determined. The expression of MyD88-TRAF6-MAPKs and PI3K/AKT pathways in neutrophils were examined.

Results: When compared with Serum_Sham, Serum_LRIP0 and Serum_LRIP1 significantly reduced the ROS released from neutrophils activated by fMLP. Meanwhile, the mRNA expression levels of NADPH oxidase subunit p22^phox and multiple ROS-producing related key proteins, such as NADPH oxidase subunit p47^phox ser 304, ser 345. MyD88, p-ERK, p-JNK and p-P38 expression of neutrophils were downregulated by Serum_LRIP0 and Serum_LRIP1. Serum_LRIP1 also downregulated p47^phox mRNA expression and tumor necrosis factor receptor-associated factor 6 (TRAF6) protein expression.

Conclusion: LRIP serum protects against ROS level and neutrophils activation involving the MyD88-TRAF6-MAPKs. This finding provides new insight into the understanding of LRIP mechanisms.

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肢体远端缺血后适应血清抑制fmlp触发的大鼠中性粒细胞激活和活性氧释放。

目的:探讨肢体远端缺血后适应(LRIP)外周血血清在降低有害再灌注损伤的活性氧(ROS)水平和中性粒细胞活化中的保护作用。方法:Sprague-Dawley大鼠左后肢5 min闭塞/5 min再灌注3个周期诱导LRIP。取血样于LRIP前或LRIP后0、1 h采集(分别命名为SerumSham、SerumLRIP0、SerumLRIP1)。测定LRIP血清对ROS水平和中性粒细胞活化的影响。检测中性粒细胞MyD88-TRAF6-MAPKs和PI3K/AKT通路的表达。结果:与SerumSham相比，SerumLRIP0和SerumLRIP1显著降低fMLP激活的中性粒细胞释放的ROS。同时，NADPH氧化酶亚基p22phox和多种ros生成相关关键蛋白，如NADPH氧化酶亚基p47phox ser 304、ser 345的mRNA表达水平。SerumLRIP0和SerumLRIP1下调中性粒细胞MyD88、p-ERK、p-JNK和p-P38的表达。血清lrip1还下调p47phox mRNA表达和肿瘤坏死因子受体相关因子6 (TRAF6)蛋白表达。结论:LRIP血清可抑制ROS水平和MyD88-TRAF6-MAPKs介导的中性粒细胞活化。这一发现为理解LRIP机制提供了新的见解。

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 生物-生化与分子生物学

CiteScore

6.10

自引率

0.00%

发文量

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.