This study aimed to investigate the role and mechanism of miR-223-3p in hypoxia/reoxygenation (H/R)-induced injury in H9c2 cardiomyocytes. An in vitro H/R injury model was established, and cells were divided into Control, H/R, H/R + Negative Control (NC), and H/R + miR-223-3p inhibitor groups. Cell viability was assessed by CCK-8 assay, miR-223-3p expression was measured via RT-qPCR, protein levels of TLR4 and phosphorylated NF-κB, p-p65 were analyzed by Western blot, and the release of inflammatory factors and lactate dehydrogenase (LDH) was detected using ELISA. The results showed that compared with the Control group, H/R treatment significantly decreased cell viability, upregulated miR-223-3p expression, and increased the levels of TLR4, p-p65, TNF-α, IL-6, and LDH. No significant difference was observed between the H/R+NC and H/R groups. However, inhibition of miR-223-3p further reduced cell viability and markedly exacerbated the expression of TLR4 and p-p65, as well as the release of inflammatory factors. These findings suggest that miR-223-3p may alleviate H/R-induced cardiomyocyte injury by negatively regulating the TLR4/NF-κB signaling pathway, whereas its inhibition aggravates inflammatory response and cellular damage, indicating its potential protective role in myocardial ischemia/reperfusion injury.

Fuqiang Kan, Lingyu Li. Protective Effect of MiR-223-3p against Hypoxia/Reoxygenation Injury in H9c2 Cardiomyocytes via Targeting the TLR4/NF-κB Pathway. International Journal of Frontiers in Medicine (2026), Vol. 8, Issue 2: 143-148. https://doi.org/10.25236/IJFM.2026.080216.

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