[Effects of microRNA-21 inhibitor on apoptosis of type II alveolar epithelial cells in rats with hyperoxia-induced acute lung injury].

OBJECTIVE: To observe the effects of microRNA-21 (miR-21) inhibitor on apoptosis of type II alveolar epithelial cells (AEC II) in rats with hyperoxia-induced acute lung injury (HALI). METHODS: Eighty Sprague-Dawley (SD) rats were divided into air-control group, hyperoxia injury group, empty-virus control group (200 μL solution with lentivirus was dropped into the nasal) and miR-21 inhibitor pretreatment group (200 μL solution with lentivirus contained miR-21 inhibitor was dropped through the nasal) by random number table. After treatment, the rats in all groups were fed in the hyperoxia incubator with oxygen concentration exceeding 90% for production of HALI model, and the rats in air-control group were fed normally without any treatment. Ten rats were selected at 0, 24, 48 and 72 hours after exposure in hyperoxia environment respectively, and the general changes of lung tissues were observed in light microscope. The right lung tissues were harvested to observe the pathological changes under light microscopy. The left lung tissues of other 10 rats in each group were harvested at 48 hours after execution, the miR-21 expression was determined by real-time fluorescence quantitative reverse transcription-polymerase chain reaction (RT-qPCR), the protein expression of cysteinyl aspartate-specific proteinase-3 (caspase-3) was determined by Western Bolt, and apoptosis of AEC II was detected by TdT-mediated dUTP nick end labeling (TUNEL). RESULTS: : 0.025±0.007 vs. 0.021±0.005) and caspase-3 (A value: 0.475±0.062 vs. 0.423±0.081) between empty-virus control group and hyperoxia injury group (both P > 0.05). (3) Compared with air-control group, the apoptosis cells in hyperoxia injury group were increased, which was further increased after pretreatment of miR-21 inhibitor, but no changes were found in empty-virus control group. CONCLUSIONS: Inhibition of miR-21 expression in vivo could aggravate the injury of lung tissue in HALI rats, and increase the apoptosis of AEC II.