MicroRNA-126 protects SH-SY5Y cells from ischemia/reperfusion injury-induced apoptosis by inhibiting RAB3IP

MicroRNA (miR)-126 is known to inhibit inflammatory responses in various inflammatory-related diseases, but its role during the cerebral ischemia/reperfusion (I/R) injury remains unknown. The present study aimed to examine the interaction between miR-126 and RAB3A interacting protein (RAB3IP), and explore its potential protective effects during I/R injury. The human neuroblastoma cell line SH-SY5Y was cultured in an oxygen-glucose deprivation/reoxygenation (OGD/R) environment to simulate I/R injury to assess miR-126 expression and cell viability. SH-SY5Y cells cultured in normal conditions were used as a negative control (NC) group. SH-SY5Y cells were transfected with a miR-126 mimic or an NC mimic, then cultured in OGD/R conditions; in rescue experiments, SH-SY5Y cells were co-transfected with RAB3IP overexpression or NC plasmid together with mimic-NC or mimic-miR, and then maintained in an OGD/R environment to evaluate miR-126, RAB3IP expression, cell viability and apoptosis. Cell viability was reduced in the Model group compared with the NC group, suggesting the successful construction of the OGD/R model. miR-126 expression was downregulated in the Model group compared with the NC group. However, following transfection with mimic-miR, cell viability increased compared with the mimic-NC group. Annexin V and PI staining and Hoechst/PI assays also indicated that apoptosis was reduced in the mimic-miR group compared with the mimic-NC group. RAB3IP expression was reduced following mimic-miR transfection. In rescue experiments, miR-126 negatively regulated RAB3IP expression; by contrast, RAB3IP did not affect that of miR-126. In addition, RAB3IP overexpression attenuated the protective effect of miR-126 on OGD/R-induced apoptosis. These findings suggest that miR-126 protects against cerebral I/R injury by targeting RAB3IP.