The aberrant expression of microRNAs (miRNAs) is associated with the pathogenesis of inflammation-related diseases. However, the biological functions of miR-21 in acute lung injury (ALI) remain largely unknown. In this study, the level of miR-21 was obviously increased, but B cell lymphoma-2 (Bcl-2) expression was markedly decreased in LPS-treated human pulmonary alveolar epithelial cells (HPAEpiC). Suppression of miR-21 attenuated LPS-induced apoptosis and inflammation in HPAEpiC and promoted the survival of mice with ALI by decreasing the inflammatory cell count, release of cytokines and permeability in lung tissues. Importantly, Bcl-2 was a direct target of miR-21, and its expression was significantly inhibited by miR-21 mimics at a post-transcriptional level. Besides, Bcl-2 over-expression reversed miR-21-induced apoptosis and inflammation status and showed synergic effects with miR-21 inhibitor in LPS-treated HPAEpiC. In conclusion, inhibition of miR-21 could ameliorate apoptosis and inflammation by restoring the expression of Bcl-2 in LPS-induced HPAEpiC and mice, which might provide therapeutic strategies for the treatment of ALI.

microRNA (miRNA) 的异常表达与炎症相关疾病的发病机制有关。然而，miR-21 在急性肺损伤 (ALI) 中的生物学功能在很大程度上仍然未知。本研究中，经LPS处理的人肺泡上皮细胞（HPAEpiC）miR-21水平明显升高，但B细胞淋巴瘤2（Bcl-2）表达明显降低。抑制 miR-21 减弱了 LPS 诱导的 HPAEpiC 细胞凋亡和炎症，并通过减少炎症细胞计数、细胞因子释放和肺组织通透性来促进 ALI 小鼠的存活。重要的是，Bcl-2 是 miR-21 的直接靶标，其表达在转录后水平被 miR-21 模拟物显着抑制。除了，Bcl-2 过表达逆转了 miR-21 诱导的细胞凋亡和炎症状态，并在 LPS 处理的 HPAEpiC 中显示出与 miR-21 抑制剂的协同作用。总之，抑制 miR-21 可以通过恢复 LPS 诱导的 HPAEpiC 和小鼠中 Bcl-2 的表达来改善细胞凋亡和炎症，这可能为 ALI 的治疗提供治疗策略。