mRNA-103 inhibition attenuates autophagy and inflammation in myocardial infarction by regulating the TLR4 pathway

Introduction This investigation determined the cardioprotective activity of mRNA-103 inhibitor against myocardial infarction (MI) and also evaluated its molecular mechanism. Material and methods MI was induced in rats by inducing myocardial ischaemia/reperfusion (I/R), and left ventricular (LV) mRNA-103 (1 × 107 TU) was injected into the myocardium around the infarcted area. The effect of mRNA-103 inhibitor was assessed by determining the levels of myocardial enzymes and cytokines in the serum, the myeloperoxidase (MPO) activity, and the levels of Toll-like receptor 4 (TLR4), nuclear factor κ-light-chain enhancer of activated B cells (NF-κB), and MyD88 mRNAs in the myocardial tissues of MI rats. Immunocytochemical analysis and a histopathology study were also performed. Results The levels of myocardial enzymes and cytokines were lower in the mRNA-103 inhibitor-treated group than in the group in which the only treatment was the induction of MI. There was a lower percentage of infarcted area and a lower apoptosis index in the mRNA-103 inhibitor-treated group compared to the MI-only. The levels of TLR4, NF-κB, and MyD88 mRNAs were lower in the myocardial tissues of the mRNA-103 inhibitor-treated group than in the MI-only group. Immunohistochemical analysis revealed that treatment with mRNA-103 inhibitor ameliorated the expression of TLR4 in the myocardial tissues of MI rats. Conclusions The data revealed that inhibition by mRNA-103 protects against myocardial injury in MI rats by regulating the inflammasome pathway.

• Publication year

  2020

• Venue

  Archives of medical science : AMS

• Publication date

  2020-02-25

• Fields of study

  Medicine

• Identifiers
  DOI 10.5114/aoms.2020.93267PMID 40190298PMCID 11969517
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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