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远程缺血预处理在大鼠中风模型中不受过度炎症的影响。

Effectiveness of remote ischaemic conditioning is not affected by hyper-inflammation in a rat model of stroke.

机构信息

Institute of Neurobiology, Biomedical Research Center of the Slovak Academy of Sciences, Soltesovej 4-6, 040 01, Kosice, Slovak Republic.

Department of Medical Physiology, Faculty of Medicine, University of Pavol Jozef Safarik, Trieda SNP 1, 040 01, Kosice, Slovak Republic.

出版信息

Sci Rep. 2024 Sep 5;14(1):20750. doi: 10.1038/s41598-024-71328-z.

DOI:10.1038/s41598-024-71328-z
PMID:39237655
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11377586/
Abstract

The inflammation and coagulopathy during coronavirus disease (COVID-19) impairs the efficiency of the current stroke treatments. Remote ischaemic conditioning (RIC) has shown potential in recent years to protect the brain and other organs against pathological conditions. This study aimed to evaluate the efficiency of RIC in brain infarct size using TTC staining and lung injury reduction by H&E staining during the hyper-inflammatory response in rats. The inflammation and coagulopathy were assessed by sedimentation rate, haematocrit, systemic oxidative stress and clotting time. Moreover, we observed changes in the cytokine profile. The results of the first part of the experiment showed that the inflammation and lung injury are fully developed after 24 h of intratracheal LPS administration. At this time, we induced focal brain ischaemia and examined the effect of RIC pre- and post-treatment. Our results showed that RIPre-C reduced the infarct size by about 23%, while RIPost-C by about 30%. The lung injury was also reduced following both treatments. Moreover, RIC modulated systemic inflammation. The level of chemokines CINC-1, LIX and RANTES decreased after 24 h of post-ischaemic reperfusion in treated animals compared to non-treated. The RIC-mediated decrease of inflammation was reflected in improved sedimentation rate and hematocrit, as well as reduced systemic oxidative stress. The results of this work showed neuroprotective and lung protective effects of RIC with a decrease in inflammation response. On the basis of our results, we assume that immunomodulation through the chemokines CINC-1, LIX, and RANTES play a role in RIC-mediated protection.

摘要

新型冠状病毒病 (COVID-19) 期间的炎症和凝血功能障碍会降低当前中风治疗的效果。远程缺血预处理 (RIC) 近年来显示出保护大脑和其他器官免受病理状态影响的潜力。本研究旨在使用 TTC 染色评估 RIC 在大鼠高炎症反应期间对脑梗死面积的影响,并通过 H&E 染色评估对肺损伤的减少作用。通过沉降率、红细胞压积、全身氧化应激和凝血时间评估炎症和凝血功能障碍。此外,我们还观察了细胞因子谱的变化。实验的第一部分结果表明,经气管内 LPS 给药 24 小时后,炎症和肺损伤完全发展。此时,我们诱导局灶性脑缺血,并检查 RIC 预处理和后处理的效果。结果表明,RICPre-C 可使梗死面积减少约 23%,而 RIPost-C 则减少约 30%。两种治疗均能减轻肺损伤。此外,RIC 调节全身炎症。与未治疗的动物相比,治疗后缺血再灌注 24 小时后趋化因子 CINC-1、LIX 和 RANTES 的水平降低。RIC 介导的炎症减少反映在沉降率和红细胞压积的改善以及全身氧化应激的降低上。这项工作的结果表明 RIC 具有神经保护和肺保护作用,并减轻炎症反应。基于我们的结果,我们假设通过趋化因子 CINC-1、LIX 和 RANTES 的免疫调节在 RIC 介导的保护中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c95/11377586/caae7ab06b55/41598_2024_71328_Fig8_HTML.jpg
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Co-evolution of SARS-CoV-2 variants and host immune response trajectories underlie COVID-19 pandemic to epidemic transition.严重急性呼吸综合征冠状病毒2(SARS-CoV-2)变体与宿主免疫反应轨迹的共同进化是新冠疫情向地方性流行转变的基础。
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