Mechanism of MiR-223 Regulating NLRP3 to Inhibit Myocardial Fibrosis in Rats with Heart Failure
10.11969/j.issn.1673-548X.2024.07.018
- VernacularTitle:miR-223调控NLRP3抑制心力衰竭大鼠心肌纤维化机制
- Author:
Peng CHAO
1
;
Yong WANG
;
Xiaoyang CHEN
Author Information
1. 830054 乌鲁木齐,新疆医科大学
- Keywords:
MiR-223;
NLRP3 inflammatory body;
Myocardial fibrosis;
Apoptosis
- From:
Journal of Medical Research
2024;53(7):88-94
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the mechanism of miR-223 regulation of Nod-like receptor protein 3(NLRP3)on myocar-dial fibrosis in rats with heart failure(HE).Methods A total of fifty-four adult Wistar rats were selected to establish rat model of con-gestive HF by abdominal aortic coarctation method,and they were divided into control group,HF group,and HF+miR-223 overexpres-sion according to random number table method,with 18 rats in each group.MiR-223mimics was injected into the tail vein of HF+miR-223 overexpression group,after transfection was successful for 72h,cardiac function related indexes of rats in each group were de-tected by animal heart color ultrasound:interventricular septal thickness at end-diastole(IVSd),left ventricular posterior wall thickness at end-diastolic(LVPWd),left ventricular end-diastolic diameter(LVEDd),left ventricular end systolic diameter(LVED)and left ventricular ejectfraction(LVEF).The heart/body ratio,lung/body ratio,liver/body ratio were calculated and measured;the expression levels of miRNA-223,NLRP3,interleukin-1β(IL-1 β),tumor necrosis factor-α(TNF-α),Collagen-3,Collagen-1,Bax,and Bcl-2 in myocardial tissue of rats in each group.Results The cardiac function of the HE group was worse than that of the control group,and the expressions of NLRP3,IL-1β,TNF-α,Collagen-1,Collagen-3 and Bax were higher than those of the control group,while the expressions of miR-223 and Bcl-2 were lower than those of the control group(P＜0.05),and the degree of myocardi-al interstitial fibrosis was significantly aggravated.The cardiac function of HF+miR-223 overexpression group was better than that of the HE group,the expressions of NLRP3,IL-1 β,TNF-α,Collagen-1,Collagen-3 and Bax were lower than those of the HE group,the expressions of miR-223 and Bcl-2 were higher than those of the HE group,and the degree of myocardial interstitial fibrosis was signifi-cantly alleviated.Conclusion MiR-223 can inhibit the expression of Collagen-1 and Collagen-3 by acting on its target NLRP3,and play an important role in the occurrence and development of myocardial fibrosis in HE.
