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)‑κB 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)‑1β, IL‑6, IL‑8, cyclooxygenase‑2, caspase‑3 and caspase‑9 levels, suppress Bax/Bcl‑2 ratio, NF‑κB 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‑κB pathway and promoting the VEGF pathway, and may develop into a therapy for ICD in future research.