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CU06-1004 enhances vascular integrity and improves cardiac remodeling by suppressing edema and inflammation in myocardial ischemia-reperfusion injury

Experimental and Molecular Medicine, 2022, 54(0), , pp.1-12 [Peer Reviewed Journal]

2021. The Author(s). ;The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2021 ;ISSN: 1226-3613 ;EISSN: 2092-6413 ;DOI: 10.1038/s12276-021-00720-w ;PMID: 34997212

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Title:
CU06-1004 enhances vascular integrity and improves cardiac remodeling by suppressing edema and inflammation in myocardial ischemia-reperfusion injury
Author: Zhang, Haiying ; Kim, Hyeok ; Park, Bong Woo ; Noh, Minyoung ; Kim, Yeomyeong ; Park, Jeongeun ; Park, Jae-Hyun ; Kim, Jin-Ju ; Sim, Woo-Sup ; Ban, Kiwon ; Park, Hun-Jun ; Kwon, Young-Guen
Subjects: Animals ; Arteries ; Blood flow ; Blood vessels ; Cardiac function ; Cardiac muscle ; Cardiomyocytes ; Cell adhesion molecules ; Cell survival ; Drug dosages ; Echocardiography ; Edema ; Edema - metabolism ; Endothelial cells ; Endothelial Cells - metabolism ; Endothelium ; Heart attacks ; Infiltration ; Inflammation ; Inflammation - drug therapy ; Inflammation - metabolism ; Ischemia ; Leukocytes (neutrophilic) ; Macrophages ; Microvasculature ; Myocardial infarction ; Myocardial ischemia ; Myocardial Reperfusion Injury - drug therapy ; Myocardial Reperfusion Injury - metabolism ; Myocytes, Cardiac - metabolism ; Oxidative stress ; Pericytes ; Rats ; Reactive oxygen species ; Reperfusion ; Saponins ; Vascular cell adhesion molecule 1 ; Ventricular Remodeling ; 생화학
Is Part Of: Experimental and Molecular Medicine, 2022, 54(0), , pp.1-12
Description: Ischemia-reperfusion (I/R) injury accelerates the cardiomyocytes (CMs) death by oxidative stress, and thereby deteriorates cardiac function. There has been a paradigm shift in the therapeutic perspective more towards the prevention or amelioration of damage caused by reperfusion. Cardiac microvascular endothelial cells (CMECs) are more vulnerable to reperfusion injury and play the crucial roles more than CMs in the pathological process of early I/R injury. In this study, we investigate that CU06-1004, as a vascular leakage blocker, can improve cardiac function by inhibiting CMEC's hyperpermeability and subsequently reducing the neutrophil's plugging and infiltration in infarcted hearts. CU06-1004 was delivered intravenously 5 min before reperfusion and the rats were randomly divided into three groups: (1) vehicle, (2) low-CU06-1004 (1 mg/kg, twice at 24 h intervals), and (3) high-CU06-1004 (5 mg/kg, once before reperfusion). CU06-1004 treatment reduced necrotic size and cardiac edema by enhancing vascular integrity, as demonstrated by the presence of intact junction proteins on CMECs and surrounding pericytes in early I/R injury. It also decreased the expression of vascular cell adhesion molecule 1 (VCAM-1) on CMECs, resulting in reduced infiltration of neutrophils and macrophages. Echocardiography showed that the CU06-1004 treatment significantly improved cardiac function compared with the vehicle group. Interestingly, single high-dose treatment with CU06-1004 provided a greater functional improvement than repetitive low-dose treatment until 8 weeks post I/R. These findings demonstrate that CU06-1004 enhances vascular integrity and improves cardiac function by preventing lethal myocardial I/R injury. It can provide a promising therapeutic option, as potential adjunctive therapy to current reperfusion strategies.
Publisher: United States: Springer Nature B.V
Language: English
Identifier: ISSN: 1226-3613
EISSN: 2092-6413
DOI: 10.1038/s12276-021-00720-w
PMID: 34997212
Source: Nature Open Access
DOAJ Directory of Open Access Journals
GFMER Free Medical Journals
MEDLINE
PubMed Central
Alma/SFX Local Collection
KoreaMed Open Access
ProQuest Central

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CU06-1004 enhances vascular integrity and improves cardiac remodeling by suppressing edema and inflammation in myocardial ischemia-reperfusion injury

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