MicroRNA-30a-3p overexpression improves sepsis-induced cell apoptosis and via the PTEN/PI3K/AKT signaling pathway.

The aim of the present study was to explain the mechanism of miR-30a-3p overexpression in sepsis-induced cell apoptosis and . For the cell experiments, H9c2 cells were divided into three groups, including the untreated normal control (NC), lipopolysaccharide (LPS)-treated and miRNA (treated with LPS and transfection with miRNA-30a-3p) groups. The cell proliferation and apoptosis were evaluated by MTT assay and flow cytometry, respectively. The relative protein expression levels were measured by western blot assay. In the experiment, a sepsis rat model was established by intraperitoneal injection of LPS. Sprague Dawley rats were divided into three groups, including the NC, LPS-injected and miRNA (in which model rats were injected with miR-30a-3p vector at the caudal vein) groups. The myocardial morphology in different groups was observed by hematoxylin and eosin staining. In addition, tissue apoptosis and protein expression levels were evaluated by TUNEL and western blot assay, respectively. The results of cell experiments indicated that the cell proliferation rate was significantly increased and the cell apoptosis rate was significantly downregulated in the miR-30a-3p group compared with the LPS group (both P<0.05). The relative protein expression of phosphatase and tensin homolog (PTEN) was markedly decreased in the miRNA group compared with the LPS group, while the levels of phosphoinositide 3-kinase (PI3K) and protein kinase B (AKT) were significantly increased in the miRNA group (all P<0.05). In the experiments, the myocardial morphology of the miRNA group was improved compared with that of the LPS group. Compared with the LPS group, cell apoptosis in the miRNA group was significantly downregulated (P<0.05), while the relative protein levels (PTEN, PI3K and AKT) in the tissues were also significantly altered (P<0.05). In conclusion, miR-30a-3p overexpression may improve the sepsis-induced cell apoptosis and via the PTEN/PI3K/AKT signaling pathway.