No abstract

Pneumonia accounts for approximately 15% mortalities in adolescents worldwide. MicroRNAs (miRNAs) regulate numerous diseases including pneumonia. miRNA and mRNA expression levels were detected by real time polymerase chain reaction (RT-qPCR). Protein expression levels were determined by enzyme-linked immunosorbent assay (ELISA) and western blot. The interaction between phosphatase and tensin homolog on chromosome ten (PTEN) and miR-103a-3p was explored by dual luciferase reporter assay. Cell viability and cell apoptosis were detected by cell Counting Kit-8 (CCK-8) and flow cytometry. Herein, we discovered that PTEN was decreased and miR-103a-3p was overexpressed in Ana-1 cells of in vitro pneumonia model. miR-103a-3p downregulated the expression levels of PTEN. AntagomiR-103a-3p reversed the increased cell apoptosis and decreased cell viability and inflammatory cytokine expression levels (tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6) induced by LPS in Ana-1 cells by PTEN. AntagomiR-103a-3p inhibited the activation of PTEN/PI3K/AKT/NF-κB signaling pathway induced by LPS in Ana-1 cells. Taken together, our findings exhibited that miR-103a-3p attenuated LPS induced pneumonia by blocking the activation of PTEN/PI3K/AKT/NF-κB signaling pathway and the following cell apoptosis as well as release of proinflammatory cytokines, suggesting that miR-103a-3p might serve as a novel therapeutic target for the treatment of pneumonia.

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide. To investigate effect of silymarin on chronic obstructive pulmonary disease (COPD). The serum samples of 20 healthy controls, 20 patients with acute exacerbation of COPD and 20 patients with stable COPD were collected. LPS and smoking were used to induce COPD mouse model. Our results showed that in patients with acute exacerbation of COPD, O2-level release from peripheral blood neutrophils were negatively correlated with forced expiratory volume in the first second (FEV1), FEV1 in predicted value, FEV1/forced vital capacity (FVC), and arterial partial pressure (PaO2). (r=-0.898, -0.878, -874, -0.890, all P<0.01). Compared with that in the control group, the phosphorylation of NADPH oxidase p47phox factor and peripheral blood neutrophil membrane protein in the stable COPD group and the acute exacerbation COPD group were significantly stronger. Silymarin can inhibit the inflammatory response and oxidative stress. In conclusion, silymarin reduces oxidative stress in phagocytic and non-phagocytic cells, thus decreasing the oxidative stress in COPD patients