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Non-thermal Infrared Light Treatment of Ischemia/Reperfusion Injury and Subsequent Analysis of Macrophage Differentiation
Published on: December 30, 2021
MicroRNA-421 improves ischemia/reperfusion injury via regulation toll-like receptor 4 pathway
Lin-Lin Guo1, Ming-Lei Guo2, Jian Yao2
1Department of Cardiology, The Affiliated Cardiovascular Hospital of Qingdao University, Qingdao, Shandong Province, China.
Objectives:
The objective was to investigate the effects of microRNA-421 against myocardial ischemia/reperfusion injury in C57BL/6 mice.
Methods:
Male C57BL/6 mice (n = 27) were randomly divided into three groups: normal control (NC) group (sham-treated); I/R model group, which underwent the I30min/R24h model (ischemia for 30 minutes followed by reperfusion for 24 hours); and the miRNA group, which were injected with miR-421. Pathology was assessed by hematoxylin and eosin staining and myocardial infarct size was measured by triphenyltetrazolium chloride staining. The apoptosis rate was measured by TUNEL assay, and relative expression of toll-like receptor-4 (TLR4), Janus kinase 2 (JAK2), and signal transducer and activator of translation 3 (STAT3) was evaluated by immunohistochemistry. Interleukin (IL)-6, tumor necrosis factor (TNF)-α, IL-10, and high mobility group protein B1 (HMGB1) serum concentrations were measured by ELISA.
Results:
Compared with the NC group, in the model group, the myocardial infarction was large; inflammatory cell infiltration was severe; apoptosis was enhanced; expression of TLR4, JAK2, and STAT3 was increased; and serum concentrations of IL-6, TNF-α, IL-10, and HMGB1 were significantly increased. In the miRNA group, the ischemia/reperfusion injury was significantly improved.
Conclusions:
Overexpression of miRNA-421 could reduce ischemia/reperfusion inflammatory response, perhaps via inactivation of TLR4, JAK2, and STAT3.
Insights
MicroRNA-421 protects against heart injury from ischemia and reperfusion. This study shows miR-421 reduces inflammation and cell death in mouse hearts, offering a potential therapeutic target.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Inflammation Research
Background:
- Myocardial ischemia/reperfusion (I/R) injury is a significant clinical problem.
- MicroRNAs (miRNAs) play crucial roles in cardiovascular diseases.
- The specific role of microRNA-421 in I/R injury needs further elucidation.
Purpose of the Study:
- To investigate the protective effects of microRNA-421 (miR-421) against myocardial I/R injury in a mouse model.
- To explore the underlying molecular mechanisms involving key inflammatory and signaling pathways.
Main Methods:
- A myocardial I/R model was established in male C57BL/6 mice.
- Mice were divided into normal control, I/R model, and miR-421 treated groups.
- Histopathology, infarct size, apoptosis, protein expression (TLR4, JAK2, STAT3), and serum cytokine levels (IL-6, TNF-α, IL-10, HMGB1) were assessed.
Main Results:
- I/R injury led to increased myocardial infarction, inflammation, and apoptosis.
- Expression of toll-like receptor-4 (TLR4), Janus kinase 2 (JAK2), and signal transducer and activator of translation 3 (STAT3) was elevated post-I/R.
- miR-421 treatment significantly ameliorated I/R-induced damage and reduced inflammatory markers.
Conclusions:
- Overexpression of miR-421 demonstrates a protective effect against myocardial I/R injury.
- miR-421 may exert its protective function by inhibiting the TLR4/JAK2/STAT3 signaling pathway.
- miR-421 represents a potential therapeutic target for mitigating I/R injury.
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