Influences of up-regulation of miR-126 on septic inflammation and prognosis through AKT/Rac1 signaling pathway

• Published in: European review for medical and pharmacological sciences Vol. 23; no. 5; p. 2132
• Main Authors: Wang, H-F, Wang, Y-Q, Dou, L, Gao, H-M, Wang, B, Luo, N, Li, Y
• Format: Journal Article
• Language: English
• Published: Italy 01.03.2019
• ISSN: 2284-0729
• DOI: 10.26355/eurrev_201903_17257

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. 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. 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. The up-regulation of miR-126 inhibited the septic inflammation and improved the prognosis of sepsis mice through the AKT/Rac1 signaling pathway.