Tanshinone IIA alleviates oxidative damage after spinal cord injury in vitro and in vivo through up-regulating miR-124

Abstract Aims Spinal cord injury (SCI) is a damage of spinal cord caused by trauma or diseases. Here, we explored the effects of tanshinone IIA (Tan IIA) on SCI oxidative damage in vitro and in vivo . Materials and methods In vitro , PC-12 cells were treated by H 2 O 2 to stimulate oxidative injury. Then, the effects of Tan IIA on cell viability, apoptosis and autophagy were assessed by CCK-8 assay, flow cytometry assay and western blotting, respectively. The expression of miR-124 was measured by qRT-PCR, and whether Tan IIA exerted effects on H 2 O 2 -treated PC-12 cells through modulating miR-124 was verified. In vivo , Sprague-Dawley rats were induced SCI using a weight drop device. Then, the effects of Tan IIA on motor function recovery of rats, myeloperoxidase (MPO) activity in damaged tissue and tissue cell proliferation, apoptosis and autophagy were investigated, respectively. Key findings In vitro , H 2 O 2 stimulation reduced cell viability, and induced cell apoptosis and autophagy. Those alterations were mitigated by Tan IIA treatment. Tan IIA treatment reversed the H 2 O 2 -induced down-regulation of miR-124. Silence of miR-124 reversed the effects of Tan IIA on H 2 O 2 -treated PC-12 cells, as well as activation of JNK and p38MAPK pathways. In vivo , Tan IIA treatment alleviated the SCI-induced enhancement of MPO activity in damaged tissue, apoptosis and autophagy of damaged tissue cells, and promoted the motor function recovery of rats. Significance Tan IIA attenuated oxidative damage after SCI in vitro and in vivo might be through up-regulating miR-124 and then inactivating JNK and p38 MAPK pathways.