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Updated: Feb 1, 2026

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
microRNA-183 improve myocardial damager via NF-kb pathway: In vitro and in vivo study
Jie Xing1, Ting Xie1, Wei Tan1
1Department of Cardiac surgery, Hainan General Hospital, Haikou, Hainan, China.
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.
Insights
MicroRNA-183 (miRNA-183) significantly reduces myocardial damage by suppressing cell apoptosis and improving cardiac pathology. This protective effect is mediated through the nuclear factor-kappa B (NF-κb) pathway.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Biochemistry
Background:
- Myocardial damage is a significant contributor to cardiovascular disease.
- MicroRNAs play crucial roles in regulating cellular processes, including apoptosis and inflammation.
- Understanding the specific roles of microRNAs in myocardial injury is essential for developing targeted therapies.
Purpose of the Study:
- To investigate the therapeutic effects of microRNA-183 (miRNA-183) on myocardial damage.
- To elucidate the underlying molecular mechanisms, particularly the involvement of the NF-κb pathway.
Main Methods:
- In vitro studies using H9C2 cells to assess apoptosis and protein expression via flow cytometry and Western blot.
- In vivo studies in a rat model of myocardial infarction to evaluate pathology, infarct size, apoptosis, and protein levels using histological and molecular techniques.
Main Results:
- miRNA-183 treatment significantly suppressed cell apoptosis in both in vitro and in vivo models.
- Histological analysis showed improved cardiac pathology and reduced infarct size in the miRNA-183 group.
- Key protein expressions, including nuclear factor-kappa B (NF-κb), caspase-3, Bax, and Bcl-2, were significantly altered by miRNA-183.
Conclusions:
- MicroRNA-183 demonstrates a protective effect against myocardial damage.
- The beneficial effects of miRNA-183 are achieved by inhibiting cell apoptosis and improving cardiac tissue integrity.
- The NF-κb pathway is identified as a key mediator of miRNA-183's cardioprotective actions.
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