Abstract

Objective: To explore the effect of miR-21-5p on the MAP2K3 expressions and cellular apoptosis in the lung tissues of neonatal rats with hyperoxia-induced lung injuries (HILI). Methods: Twenty Sprague-Dawley neonatal rats were assigned to the normal group, and 120 rats were used to create a HILI model and were divided into the following six groups of 20 rats each: the model group, the miR-21-5p NC group, the miR-21-5p agomir group, the oe-NC group (MAP2K3 overexpression NC), the oe-MAP2K3 group, and the miR-21-5p agomir+oe-MAP2K3 group. Results: miR-21-5p can target MAP2K3. Compared with the normal rats, the rats with HILI had lower miR-21-5p expression levels and higher MAP2K3 expression levels in the lung tissues (both P<0.05). Unlike the normal group, the other groups all presented different degrees of lung injuries, lower Bcl-2 expression levels, higher cellular apoptosis rates, and higher expression levels of cleaved caspase-3, Bax, IL-6, and TNF-α (all P<0.05). Compared with the model and the miR-21-5p NC groups, the miR-21-5p agomir group had better results in terms of the aforementioned markers; compared with the oe-NC group, the oe-MAP2K3 group had worse results in terms of these markers (all P<0.05). Moreover, we found that the protective effects of miR-21-5p overexpression on the lung tissues of HILI rats can be partially blocked by MAP2K3 overexpression. Conclusion: miR-21-5p can inhibit MAP2K3 expression and reduce cellular apoptosis in HILI, thereby exerting protective effects on neonatal rats with HILI.