MiR-124 inhibits neural apoptosis in ischemic stroke

Stroke is a common disease around the world, which causes cerebral tissue damage due to rupture or occlusion of cerebral vessels. Previous studies showed that a large number of microRNA was involved in post-stroke damage or regeneration of neural tissue, among which miR-124 was reported to play a pivotal role in neural differentiation. Our study was focused on the expression of miR-124 in ischemic stroke and the effect of miR-124 on neural apoptosis. 40 male C57BL6 mice were prepared for establishment of cerebral infarction model with suture method. Tissues of stroke lesion were extracted for examination of miR-124 expression by qRT-PCR and in situ molecular hybridization. Mice neurons were cultured in vitro and transfected with lentiviral expression vector of miR-124. Proliferation of neurocytes was assessed by MTT assays. Western-Blot was performed to examine the expression of Bcl-2, P53 and Caspase-3. Our results showed cerebral infarction model was successfully established as demonstrated by significant infarcted lesion. qRT-PCR and in situ molecular hybridization showed that, compared with normal tissues, tissues of stroke lesion had a higher expression of miR-124 (P<0.01). Overexpression of miR-124 up-regulated apoptosis-associated Bcl-2 expression (P<0.05), inhibited expression of activated caspase-3 (P<0.05), and enhanced proliferation of neurocytes (P<0.05). In conclusion, miR-124 was up-regulated in infarcted tissues after ischemic stroke. MiR-124 inhibited neural apoptosis and enhanced proliferation of neurocytes via apoptosis-associated pathways.