Geomagnetic activity affects animal myocardial ischemia/reperfusion injury: an experimental-simulated study

Author:

Chang Weiyu,Chen Xinli,Yang Yuan,Deng Yanglin,Dong Liang,Wu HuiORCID

Abstract

AbstractNumerous studies have shown that geomagnetic activity (GMA) contributes to the development and escalation of cardiovascular disease (CVD), as well as increased morbidity and mortality. However, the underlying molecular mechanisms and approaches for understanding GMA remain unclear. This study aimed to investigate the impact of GMA on oxidative stress and inflammatory responses. Myocardial ischemia/reperfusion injury (MI/RI) rat models were created under various geomagnetic field conditions. The range of cardiac function, markers of myocardial injury, inflammatory factors, and the TLR4/NF-κB signaling pathway were measured after the 24-h period. The findings showed that weak GMA significantly improved cardiac function in the MI/RI rat model and reduced the size of myocardial infarction and creatine kinase (CK) and lactic dehydrogenase (LDH) levels. Additionally, weak GMA enhanced superoxide dismutase (SOD) activity and decreased malondialdehyde (MDA) content. Furthermore, weak GMA significantly reduced the levels of the myocardial inflammatory cytokines interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). Conversely, the effects observed under severe GMA conditions were opposite to those observed under weak GMA. Western blot and qPCR analysis demonstrated that weak GMA led to a significant downregulation of TLR4, TRAF6, NF-κB, TNF-α, and MCP-1 in the MI/RI rat models. In contrast to weak GMA, severe GMA increased TLR4, TRAF6, NF-κB, and TNF-α expression. This study suggested that weak GMA had a limiting effect on MI/RI rat models, whereas severe GMA exacerbated injury in MI/RI rats. These effects were associated with oxidative stress and inflammatory responses and might potentially involve the TLR4/NF-κB signaling pathway.

Funder

National Natural Science Foundation of China

High-level Health Personnel Training Project of Yunnan Province

Publisher

Springer Science and Business Media LLC

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3