MicRNA-320 facilitates the brain parenchyma injury via regulating IGF-1 during cerebral I/R injury in mice

Abstract

Purpose: To investigate the protective effects of miR-320 on cerebral ischemia/reperfusion (I/R) injury in mice and PC12 cells.

Methods: miR-320 normal control (NC), inhibitor fragment and overexpression fragments were injected into mice lateral ventricles. Thereafter, the middle cerebral artery occlusion (MCAO) for left cerebrum method was employed in order to establish a cerebral I/R injury mice model. Apoptosis in the peripheral region of cerebral infarction and the volume of cerebral infarction and brain edema were tested as well. For simulating MCAO in vitro, the PC12 cells were subjected to oxygen-glucose deprivation. The lentivirus transfection technique was used to overexpress or inhibit miR-320. Furthermore, the effects of miR-320 on the survival and apoptosis of PC12 were monitored by MTT and TUNEL detection.

Results: A cerebral I/R injury mice model was successfully established. MiR-320 enhanced cell apoptosis of the injury side cortical infarcted peripheral zone and increased brain infarction volume and edema volume in MCAO/R mice. In addition, Insulin growth factor-1 (IGF-1) mRNA and protein expressions in MCAO/R mice were inhibited by miR-320 as well. Moreover, the results of cell studies were consist with the animal studies.

Conclusions: miR-320 may be involved in the regulation of cerebral I/R for brain parenchyma injury by inhibition of IGF-1 pathway.

Keywords: Apoptosis; IGF-1; Ischemia/reperfusion; miR-320.