吡喃结构域
炎症体
医学
炎症
免疫印迹
巨噬细胞
体内
心肌梗塞
药理学
内科学
特拉尼司特
免疫学
体外
化学
生物
生物化学
基因
生物技术
作者
Di Qu,Huihui Guo,Yanan Xu
出处
期刊:Journal of Interferon and Cytokine Research
[Mary Ann Liebert]
日期:2021-03-01
卷期号:41 (3): 102-110
被引量:3
标识
DOI:10.1089/jir.2020.0208
摘要
Acute myocardial infarction (AMI) has been a devastating actuality and accounts for half of cardiovascular emergency department visits. Nucleotide oligomerization domain, leucine-rich repeat, and pyrin domain-containing protein 3 (NLRP3) inflammasome participates in the mediation of myocardial inflammation during AMI. Therefore, this study aimed to reveal the therapeutic function of tranilast, an agent targeting NLRP3, for AMI. AMI mouse model was first established by transient myocardial ischemia. Western blot and quantitative reverse transcription polymerase chain reaction assay were performed to estimate the expression levels of related genes. Flow cytometry was used to analyze the macrophage types, and the therapeutic effects of tranilast were estimated by echocardiographic analysis and Masson's trichrome stain. We demonstrated that AMI induced the activation of NLRP3 inflammasome in the heart tissues of mice with AMI. Tranilast decreased the expression of interleukin-1β and cleaved caspase-1 in bone marrow-derived macrophages and thus re-educated M1-macrophages toward the M2-phenotype both in vitro and in vivo. Tranilast inhibited the activation in the heart tissues of AMI mice and thus improved cardiac functional recovery in the AMI mouse model. In conclusion, we revealed that tranilast ameliorated myocardial infarction by inhibiting NLRP3 inflammasome and re-educating macrophage phenotype in this study.
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