microRNA‐183 improve myocardial damager via NF‐kb pathway: In vitro and in vivo study

Abstract

Aim: The aim of this study is to evaluate the effects of microRNA-183 (miRNA-183) in myocardial damager.Methods: In the cell experiment, the H9C2 cell was divided into three groups: NC group, Model group, and miRNA group. The cell apoptosis and relative proteins' expressions were measured by flow cytometry and Western blot assay. The in vivo study of the rats was divided into three groups: Sham group, Model group, and miRNA group. The pathology, Infarct size, cell apoptosis, and relative protein expressions were evaluated by hematoxylin and eosin staining, nitro blue tetrazolium staining, terminal deoxynucleotidyl transferase dUTP nick-end labeling assay, and immunohistochemistry. Results: Compared with NC groups, the in vitro and in vivo study showed that cell apoptosis rate of miRNA groups was significantly suppressed (P < 0.05). The pathology and infarct size of miRNA group were significantly improved compared with the NC group. Meanwhile, the relative proteins expression (nuclear factor-κB [NF-kb], caspase-3, Bax, and Bcl-2) of miRNA groups were significantly different compared with those of NC groups (P < 0.05). Conclusion:In vitro and in vivo study revealed that miRNA-183 improves myocardial damager through the NF-κb pathway.

MiR‐27 alleviates myocardial cell damage induced by hypoxia/reoxygenation via targeting TGFBR1 and inhibiting NF‐κB pathway

“…Many reports illustrated that many miRNAs have effects on NF‐κB pathway . According to Xing et al, miRNA‐183 could improve myocardial damage via NF‐κB signaling . Thus far, previous study has confirmed that upregulation of miR‐27 suppressed the pathogenesis of osteoarthritis by inactivating the NF‐κB pathway .…”

“…32,33 According to Xing et al, miRNA-183 could improve myocardial damage via NF-κB signaling. 34 Thus far, previous study has confirmed that upregulation of miR-27 suppressed the pathogenesis of osteoarthritis by inactivating the NF-κB pathway. 35 It has found that IL-6 and TNF-α are important target genes in NF-κB signaling pathway.…”

MiR‐16, as a potential NF‐κB‐related miRNA, exerts anti‐inflammatory effects on LPS‐induced myocarditis via mediating CD40 expression: A preliminary study

“…Several studies have shown that many miRNAs have effects on the NF‐κB pathway . A previous study confirmed that miRNA‐183 could relieve myocardial damage via the NF‐κB pathway . It has been shown that the upregulation of gga‐miR‐16‐5p repressed the proliferation of mycoplasma gallisepticum‐infected fibroblast cells by PI3K/Akt/NF‐κB inactivation .…”

Rapid changes of miRNAs-20, -30, −410, −515, −134, and −183 and telomerase with psychological activity: A one year study on the relaxation response and epistemological considerations

“… 33 The miRNAs −20, 22 , 29 −30, 34 −410, 35 −515, 34 −134, 23 −183 36 , 37 met all these characteristics. 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54…”