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Erschienen in: Cardiovascular Drugs and Therapy 4/2019

06.07.2019 | ORIGINAL ARTICLE

Resolvin D1 Attenuates Myocardial Infarction in a Rodent Model with the Participation of the HMGB1 Pathway

verfasst von: Rui Liu, Zhenkun Li, Qiang Wang

Erschienen in: Cardiovascular Drugs and Therapy | Ausgabe 4/2019

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Abstract

Purpose

Myocardial infarction (MI) is associated with high morbidity and mortality worldwide. This study aimed to explore the roles of resolvin D1 (RvD1), a metabolite of omega-3 polyunsaturated fatty acids, in protection against MI and investigate its influences on high mobility group box 1 protein (HMGB1) and related molecular mechanisms.

Methods

Three-month-old male Sprague–Dawley rats were divided into five groups: sham, MI, MI+0.02 μg RvD1, MI+0.1 μg RvD1, and MI+0.3 μg RvD1. Vehicle control or different doses of RvD1 were injected into the left ventricle (LV) cavity 5 min before MI induction. During MI induction, myocardial ischemia lasted for 45 min followed by 180 min of reperfusion. After the reperfusion, blood and LV samples were collected for biochemical examination.

Results

The MI group produced a significant increase in myocardial infarct size, serum cardiac biomarkers (LDH and CK-MB), proinflammatory cytokines (TNF-α and IL-6), and MDA levels, and a significant decrease in SOD level compared with the sham group. Moreover, a significant upregulation of gene and protein expressions of HMGB1 and its related TLR4 and NF-κB were observed in the MI group when compared with the sham group. Pretreatment of RvD1 ameliorated the biochemical changes caused by MI.

Conclusions

Our results suggested that RvD1 pretreatment exhibited protective effects against MI through downregulation of HMGB1 and its related TLR4 and NF-κB expressions.
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Metadaten
Titel
Resolvin D1 Attenuates Myocardial Infarction in a Rodent Model with the Participation of the HMGB1 Pathway
verfasst von
Rui Liu
Zhenkun Li
Qiang Wang
Publikationsdatum
06.07.2019
Verlag
Springer US
Erschienen in
Cardiovascular Drugs and Therapy / Ausgabe 4/2019
Print ISSN: 0920-3206
Elektronische ISSN: 1573-7241
DOI
https://doi.org/10.1007/s10557-019-06884-y

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