MicroRNA-132 modifies angiogenesis in patients with ischemic cerebrovascular disease by suppressing the NF-κB and VEGF pathway

In the present study, the expression of microRNA (miR)-132 and the mechanism by which it modifies angiogenesis in patients with ischemic cerebrovascular disease (ICD) was investigated. RNA isolation and reverse transcription-quantitative polymerase chain reaction were used to measure miR-132 expression in patients with ICD. Inflammatory factors were measured using ELISA kits and western blotting measured B-cell lymphoma-2 (Bcl-2)-associated X/Bcl-2 ratio (Bax/Bcl-2 ratio), nuclear factor (NF)-kappa B p65, matrix metalloproteinase-9 (MMP-9), vascular cell adhesion molecule-1 (VCAM-1) and protein expression of inducible nitric oxide synthase (iNOS), and vascular endothelial growth factor (VEGF) protein expression. miR-132 expression in patients with ICD was lower compared with healthy volunteers. PC12 cells were used to create an oxygen glucose deprivation (OGD) model. miR-132 overexpression in an in vitro model was able to reduce tumor necrosis factor-a, interleukin (IL)-1 beta, IL-6, IL-8, cyclooxygenase-2, caspase-3 and caspase-9 levels, suppress Bax/Bcl-2 ratio, NF-kappa B p65, MMP-9, VCAM-1, iNOS, VEGF protein expression. The results suggested that miR-132 may modify angiogenesis in patients with ICD by suppressing the NF-kappa B pathway and promoting the VEGF pathway, and may develop into a therapy for ICD in future research.