Literature DB >> 34956463

17-estradiol nanoparticles influence inflammatory response of myocardial infarction possibly through downregulation of miR-302b.

Hao Ma1, Dong Xu1, Fei Liu1, Qing Yao1.   

Abstract

Cardiovascular death is increasing year by year, and effective treatment is a challenging clinical problem at present. The application of nano materials has pointed to a new therapeutic direction for the clinical treatment of cardiovascular diseases, and preparation of nanoparticles (NPs) with PBCA as carrier material has become a trending spot in clinical research. In this study, we observed the influence of 17-estradiol nanoparticles (17-E2-NPs) on the inflammatory response of myocardial infarction (MI) and its regulatory effect on miR-302b. First of all, we enrolled MI patients and healthy controls, and preliminarily determined that miR-302b was highly expressed in MI and positively correlated with inflammation response. Then, we prepared 17-E2-NPs and purchased rats for modeling to analyze the underlying mechanism of action. The results showed that in rats treated with 17-E2-NPs, the expression of miR-302b and inflammatory cytokines decreased, the proliferation of cardiac fibroblasts reduced and the apoptosis rate increased. According to the above results, we conclude that 17-E2-NPs can inhibit the proliferation of cardiac fibroblasts, promote the apoptosis rate and reduce the inflammatory reaction of MI, via the downregulation of miR-302b, which may be one of the effective treatment schemes for MI in the future. AJTR
Copyright © 2021.

Entities:  

Keywords:  17-estradiol nanoparticles; inflammatory response; miR-302b; myocardial infarction

Year:  2021        PMID: 34956463      PMCID: PMC8661167     

Source DB:  PubMed          Journal:  Am J Transl Res        ISSN: 1943-8141            Impact factor:   4.060


  31 in total

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9.  The effect of estrogen on hepatic microcirculation after ischemia/reperfusion.

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Review 10.  Mortality and morbidity trends after the first year in survivors of acute myocardial infarction: a systematic review.

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