MiR-195 alleviates oxygen-glucose deprivation/reperfusion-induced cell apoptosis via inhibition of IKKα-mediated NF-κB pathway

Objectives: Increasing evidence confirmed that miRNA plays a critical role in the occurrence and development of ischemic stroke. Here, the aim of this study was to examine the function and mechanisms of miR-195 in vascular endothelial cell apoptosis induced by oxygen-glucose deprivation (OGD). Methods: This study intended to use OGD to simulate ischemia in vitro. The mRNA expression of miR-195, IKK alpha and NF-kappa B in human umbilical vein endothelial cells (HUVECs) were detected by RT-qPCR. The proliferation and apoptosis ability of HUVECs were evaluated using MTT assay, colony formation assay and flow cytometry, respectively. Western blot was applied to examine related protein expression. The interaction between miR-195 and IKK alpha was verified by dual-luciferase reporter gene assay. Results: OGD significantly inhibited cell viability and induced cell apoptosis in HUVECs. Meanwhile, OGD treatment notably decreased the expression of miR-195, as well as enhanced NF-kappa B expression. Moreover, miR-195 directly interacted with IKK alpha and suppressed its expression. Mechanically, overexpression of miR-195 exhibited pro-proliferation and anti-apoptotic effect on HUVECs treated with OGD through targeting IKK alpha-mediated NF-kappa B pathway. At the molecular level, through suppressing IKK alpha/NF-kappa B pathway, miR-195 inhibited the expression of pro-apoptotic protein Bax and active caspase-3, but increased the expression of anti-apoptotic Bcl-2 in HUVECs. Conclusions: Our finding uncovers the protective effect of miR-195 on the biological behavior of HUVECs via suppression of the NF-kappa B pathway induced by IKK alpha, which may provide a new potential strategy for ischemic stroke clinical treatment.