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通过肢体节律性压迫进行远程预处理通过下调炎症A2腺苷受体减轻心肌梗死

Remote Conditioning by Rhythmic Compression of Limbs Ameliorated Myocardial Infarction by Downregulation of Inflammation A2 Adenosine Receptors.

作者信息

Xu Senlei, Gu Renjun, Bian Xiangyu, Xu Xin, Xia Xuefeng, Liu Yuchen, Jia Chengjie, Gu Yihuang, Zhang Hongru

机构信息

School of Acupuncture and Tuina, School of Regimen and Rehabilitation, Nanjing University of Chinese Medicine, Nanjing, China.

Key Laboratory of Acupuncture and Medicine Research of Ministry of Education, Nanjing University of Chinese Medicine, Nanjing, China.

出版信息

Front Cardiovasc Med. 2022 Apr 8;8:723332. doi: 10.3389/fcvm.2021.723332. eCollection 2021.

DOI:10.3389/fcvm.2021.723332
PMID:35498376
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9040771/
Abstract

BACKGROUND

Remote ischemic conditioning (RIC) is a cardioprotective phenomenon, yet transient ischemia is not a requisite trigger for remote cardioprotection. In fact, RIC is a stimulus compound containing interruption of the blood vessel and tissue compression. In this study, we evaluate the effects of remote tissue compression on infarct size after myocardial infarction and explore its preliminary mechanisms.

METHODS AND RESULTS

We used a murine model of myocardial infarction to assess ischemia injury and identified remote conditioning by rhythmic compression on forelimb as a novel cardioprotective intervention. We show that the cardioprotective signal transduction of remote conditioning from the trigger limb to the heart involves the release of adenosine. Our results demonstrate that A2a and A2b receptors are indispensable parts for cardioprotection of remote conditioning, which is linked to its anti-inflammatory properties by the subsequent activation of cAMP/PKA/NF-κB axis.

CONCLUSION

Our results establish a new connection between remote tissue compression and cardiovascular diseases, which enhances our cognition about the role of tissue compression on RIC cardioprotection.

摘要

背景

远程缺血预处理(RIC)是一种心脏保护现象,但短暂性缺血并非远程心脏保护的必要触发因素。事实上,RIC是一种包含血管中断和组织压迫的复合刺激。在本研究中,我们评估了远程组织压迫对心肌梗死后梗死面积的影响,并探讨其初步机制。

方法与结果

我们使用小鼠心肌梗死模型评估缺血损伤,并将通过对前肢进行节律性压迫来确定远程预处理作为一种新型心脏保护干预措施。我们发现,从触发肢体到心脏的远程预处理的心脏保护信号转导涉及腺苷的释放。我们的结果表明,A2a和A2b受体是远程预处理心脏保护不可或缺的部分,其通过随后激活cAMP/PKA/NF-κB轴与其抗炎特性相关联。

结论

我们的结果建立了远程组织压迫与心血管疾病之间的新联系,这增强了我们对组织压迫在RIC心脏保护中作用的认识。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a85c/9040771/878bc8ec6fe2/fcvm-08-723332-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a85c/9040771/d589e3872967/fcvm-08-723332-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a85c/9040771/57d8eae23aca/fcvm-08-723332-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a85c/9040771/8d718d23a750/fcvm-08-723332-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a85c/9040771/2f3e2db8b49e/fcvm-08-723332-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a85c/9040771/c3bead2c9aed/fcvm-08-723332-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a85c/9040771/08e519f08f23/fcvm-08-723332-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a85c/9040771/878bc8ec6fe2/fcvm-08-723332-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a85c/9040771/d589e3872967/fcvm-08-723332-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a85c/9040771/57d8eae23aca/fcvm-08-723332-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a85c/9040771/8d718d23a750/fcvm-08-723332-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a85c/9040771/2f3e2db8b49e/fcvm-08-723332-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a85c/9040771/c3bead2c9aed/fcvm-08-723332-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a85c/9040771/08e519f08f23/fcvm-08-723332-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a85c/9040771/878bc8ec6fe2/fcvm-08-723332-g0007.jpg

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