OBJECTIVE: To explore the influences of the up-regulation of micro ribonucleic acid (miR)-126 on septic inflammation and prognosis through the AKT/Rac1 signaling pathway. MATERIALS AND METHODS: Human pulmonary microvascular endothelial cells (HMVECs) were cultured and transfected with miR-126 mimics. The HMVECs in the logarithmic growth phase in different groups were incubated with thrombin. The transmembrane resistivity of HMVECs was detected as the permeability via Electric Cell-substrate Impedance Sensing (ECIS) system. The endothelial cell space was observed via immunofluorescence. The mouse model of sepsis was then established and the serum was extracted to detect interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). The survival curve was plotted based on the death time. The Statistical Product and Service Solutions (SPSS) 22.0 was used for statistical analysis, and p<0.05 suggested that the difference was statistically significant. RESULTS: Thrombin could significantly increase the permeability of HMVECs, while the overexpression of miR-126 markedly inhibited the increased permeability. The overexpression of miR-126 also reduced the endothelial cell space induced by thrombin. In addition, the serum IL-6 and TNF-α levels of sepsis mice in miR-126 overexpression group were significantly decreased compared to those in the control group. Moreover, the death rate of mice exogenously expressing miR-126 was lower than that in the control group. CONCLUSIONS: The up-regulation of miR-126 inhibited the septic inflammation and improved the prognosis of sepsis mice through the AKT/Rac1 signaling pathway.
OBJECTIVE: To explore the influences of the up-regulation of micro ribonucleic acid (miR)-126 on septic inflammation and prognosis through the AKT/Rac1 signaling pathway. MATERIALS AND METHODS:Human pulmonary microvascular endothelial cells (HMVECs) were cultured and transfected with miR-126 mimics. The HMVECs in the logarithmic growth phase in different groups were incubated with thrombin. The transmembrane resistivity of HMVECs was detected as the permeability via Electric Cell-substrate Impedance Sensing (ECIS) system. The endothelial cell space was observed via immunofluorescence. The mouse model of sepsis was then established and the serum was extracted to detect interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). The survival curve was plotted based on the death time. The Statistical Product and Service Solutions (SPSS) 22.0 was used for statistical analysis, and p<0.05 suggested that the difference was statistically significant. RESULTS:Thrombin could significantly increase the permeability of HMVECs, while the overexpression of miR-126 markedly inhibited the increased permeability. The overexpression of miR-126 also reduced the endothelial cell space induced by thrombin. In addition, the serum IL-6 and TNF-α levels of sepsismice in miR-126 overexpression group were significantly decreased compared to those in the control group. Moreover, the death rate of mice exogenously expressing miR-126 was lower than that in the control group. CONCLUSIONS: The up-regulation of miR-126 inhibited the septic inflammation and improved the prognosis of sepsismice through the AKT/Rac1 signaling pathway.