EXPERIMENTAL RESEARCH
mRNA-103 inhibition attenuates autophagy and inflammation in myocardial infarction by regulating the TLR4 pathway
Fan Li 1,   XiaoHui Ma 2,   Tong Liu 3, 4,   Yang Wang 3, 4,   Xin Xie 5,   Yi Xin 6,   Kang Cheng 3, 4
 
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1
A1School of Life Science, Northwest University, Xian, China
2
Department of Vascular Surgery, General Hospital of PLA, Beijing, China
3
Department of Cardiology, Affiliated Hospital of Northwest University, Xian, China
4
Department of Cardiology, Xian No. 3 Hospital, Xian, China
5
Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, College of Life Science, Northwest University, Xian, China
6
School of Life Science, Beijing Institute of Technology, Beijing, China
Submission date: 2019-11-09
Final revision date: 2020-01-15
Acceptance date: 2020-01-31
Online publication date: 2020-02-25
 
 
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ABSTRACT
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-B, 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.

eISSN:1896-9151
ISSN:1734-1922