MicroRNA­126 protects SH­SY5Y cells from ischemia/reperfusion injury­induced apoptosis by inhibiting RAB3IP.

ABSTRACT

MicroRNA (miR)­126 is known to inhibit inflammatory responses in various inflammatory­related diseases, but its role during the cerebral ischemia/reperfusion (I/R) injury remains unknown. The present study aimed to examine the interaction between miR­126 and RAB3A interacting protein (RAB3IP), and explore its potential protective effects during I/R injury. The human neuroblastoma cell line SH­SY5Y was cultured in an oxygen­glucose deprivation/reoxygenation (OGD/R) environment to simulate I/R injury to assess miR­126 expression and cell viability. SH­SY5Y cells cultured in normal conditions were used as a negative control (NC) group. SH­SY5Y cells were transfected with a miR­126 mimic or an NC mimic, then cultured in OGD/R conditions; in rescue experiments, SH­SY5Y cells were co­transfected with RAB3IP overexpression or NC plasmid together with mimic­NC or mimic­miR, and then maintained in an OGD/R environment to evaluate miR­126, 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. miR­126 expression was downregulated in the Model group compared with the NC group. However, following transfection with mimic­miR, cell viability increased compared with the mimic­NC group. Annexin V and PI staining and Hoechst/PI assays also indicated that apoptosis was reduced in the mimic­miR group compared with the mimic­NC group. RAB3IP expression was reduced following mimic­miR transfection. In rescue experiments, miR­126 negatively regulated RAB3IP expression; by contrast, RAB3IP did not affect that of miR­126. In addition, RAB3IP overexpression attenuated the protective effect of miR­126 on OGD/R­induced apoptosis. These findings suggest that miR­126 protects against cerebral I/R injury by targeting RAB3IP.