Methylprednisolone effects on the migration of endogenous neural stem cells after spinal cord injury / 中国组织工程研究

ABSTRACT

BACKGROUND:After spinal cord injury, endogenous neural stem cel s are activated to proliferate and migrate to repair damaged tissue. As a clinical medicine, methylprednisolone shows a lot of functions, but its effects on endogenous neural stem cel s are stil unknown. OBJECTIVE:To explore the effects of methylprednisolone on the proliferation and migration of endogenous neural stem cel s after spinal cord injury. METHODS:Seventy-five Sprague-Dawley rats were used to make animal models of T10 complete paraplegia using Al en’s method, and randomized into methylprednisolone, normal saline and model groups. Rats in these three groups were given intraperitoneal injection of 1 g/L methylprednisolone solution at a dose of 30 mg/kg for 10 minutes and at a dose of 5.4 mg/kg/h for 23 hours, given intraperitoneal injection of normal saline at the same dose and given no treatment, respectively. Neurological and motor functions were assessed by somatosensory evoked potential and Basso Beattie Bresnahan scores at 7, 14, 21, 28 days after spinal cord injury. BrdU and Nestin staining of the injured spinal cord segment was conducted. RESULTS AND CONCLUSION:A large amount of BrdU-and Nestin-positive cel s were visible in al the groups, and the number of these cel s reached the peach at 14 days after spinal cord injury. Methylprednisolone was found to inhibit BrdU-, Nestin-or double-positive cel s, indicating methylprednisolone can inhibit the proliferation and migration of endogenous neural stem cel s. The results of Basso Beattie Bresnahan scores showed no notable improvement in the motor function of the limbs. Methylprednisolone also showed no significant effects on the motor evoked potential latency, but promoted nerve conduction recovery. Al these findings indicate that methylprednisolone has some hindering effects on spinal cord repair by inhibiting the proliferation and migration of endogenous neural stem cel s after spinal cord injury.