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CXCR4 拮抗剂 DBPR807 对大鼠和猪心肌梗死缺血再灌注损伤的保护作用:经皮冠状动脉介入治疗的潜在辅助治疗。

Protective Effect of CXCR4 Antagonist DBPR807 against Ischemia-Reperfusion Injury in a Rat and Porcine Model of Myocardial Infarction: Potential Adjunctive Therapy for Percutaneous Coronary Intervention.

机构信息

Institute of Biotechnology and Pharmaceutical Research, National Health Research Institutes, Zhunan 35053, Taiwan.

Taipei Heart Institute, Taipei Medical University, Taipei 11031, Taiwan.

出版信息

Int J Mol Sci. 2022 Oct 3;23(19):11730. doi: 10.3390/ijms231911730.


DOI:10.3390/ijms231911730
PMID:36233031
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9570210/
Abstract

CXCR4 antagonists have been claimed to reduce mortality after myocardial infarction in myocardial infarction (MI) animals, presumably due to suppressing inflammatory responses caused by myocardial ischemia-reperfusion injury, thus, subsequently facilitating tissue repair and cardiac function recovery. This study aims to determine whether a newly designed CXCR4 antagonist DBPR807 could exert better vascular-protective effects than other clinical counterparts (e.g., AMD3100) to alleviate cardiac damage further exacerbated by reperfusion. Consequently, we find that instead of traditional continuous treatment or multiple-dose treatment at different intervals of time, a single-dose treatment of DBPR807 before reperfusion in MI animals could attenuate inflammation via protecting oxidative stress damage and preserve vascular/capillary density and integrity via mobilizing endothelial progenitor cells, leading to a desirable fibrosis reduction and recovery of cardiac function, as evaluated with the LVEF (left ventricular ejection fraction) in infarcted hearts in rats and mini-pigs, respectively. Thus, it is highly suggested that CXCR4 antagonists should be given at a single high dose prior to reperfusion to provide the maximal cardiac functional improvement. Based on its favorable efficacy and safety profiles indicated in tested animals, DBPR807 has a great potential to serve as an adjunctive medicine for percutaneous coronary intervention (PCI) therapies in acute MI patients.

摘要

趋化因子受体 4 拮抗剂已被声称可降低心肌梗死(MI)动物的死亡率,推测是由于抑制了心肌缺血再灌注损伤引起的炎症反应,从而促进组织修复和心功能恢复。本研究旨在确定一种新设计的趋化因子受体 4 拮抗剂 DBPR807 是否比其他临床对照药物(如 AMD3100)具有更好的血管保护作用,以进一步减轻再灌注引起的心脏损伤。因此,我们发现,与传统的连续治疗或不同时间间隔的多次剂量治疗不同,在 MI 动物再灌注前单次给予 DBPR807 治疗可以通过保护氧化应激损伤来减轻炎症,并通过动员内皮祖细胞来维持血管/毛细血管密度和完整性,从而导致理想的纤维化减少和心功能恢复,分别用大鼠和小型猪的梗死心脏中的 LVEF(左心室射血分数)进行评估。因此,强烈建议在再灌注前给予趋化因子受体 4 拮抗剂单次高剂量,以提供最大的心功能改善。基于在试验动物中显示的良好疗效和安全性特征,DBPR807 有可能成为急性 MI 患者经皮冠状动脉介入治疗(PCI)的辅助药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/ee53b5517710/ijms-23-11730-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/eab38ce8ff87/ijms-23-11730-g0A1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/1ab5ce2faa64/ijms-23-11730-g0A2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/9bda55ee8292/ijms-23-11730-g0A3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/641d7800ce14/ijms-23-11730-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/ef58d9397332/ijms-23-11730-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/78541f308dba/ijms-23-11730-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/41e5a79ac697/ijms-23-11730-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/b83e5ecc4033/ijms-23-11730-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/a6d4977243ce/ijms-23-11730-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/ee53b5517710/ijms-23-11730-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/eab38ce8ff87/ijms-23-11730-g0A1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/1ab5ce2faa64/ijms-23-11730-g0A2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/9bda55ee8292/ijms-23-11730-g0A3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/641d7800ce14/ijms-23-11730-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/ef58d9397332/ijms-23-11730-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/78541f308dba/ijms-23-11730-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/41e5a79ac697/ijms-23-11730-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/b83e5ecc4033/ijms-23-11730-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/a6d4977243ce/ijms-23-11730-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b16/9570210/ee53b5517710/ijms-23-11730-g007.jpg

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