The Effects of miR-30a and miR-17 Biomarkers and Methylprednisolone in Experimental Spinal Cord Injury in Rats

Abstract

Introduction: Methylprednisolone, is a neuroprotective steroid with many effective mechanisms such as inflammation, cell blood flow changes, and apoptosis in the early period following spinal cord injury. This study aimed to demonstrate the inhibitory activity of methylprednisolone to prevent early injury through microRNA expressions, which are predicted to play a role in genomic regulation.

Method: This present study was conducted on 56 male Sprague-Dawley rats. All the animals divided into 8 groups which consists of 7 animals each. Laminectomy procedure was performed between levels T5-8. All the groups except the two control groups have been damaged with the Yasargil aneurysm clip for 1 minute at the T5 level. T5-8 spinal cord tissue was removed at the 6th, 12th, and 24th hours after clipping. Methylprednisolone was given to the intraperitoneal cavity only to the clipped groups. As a result of histopathological and immunohistochemical examination, there was a significant decrease in cell necrosis, edema, hemorrhage and white matter-gray matter transition in groups given methylprednisolone. Damaged spinal cord samples excised from all rats. miR-30a and miR-17 gene expression levels were evaluated by quantative PCR method.

Results: miR-30a was significantly upregulated at 12th and 24th hours after spinal cord injury and this rise  was restricted  in the methylprednisolone treated groups.. miR-17 was down-regulated at the 6th hour and and reached its lowest level at the 12th hour.

Conclusion: Methylprednisolone has statistically significant healing effects on spinal cord injury through the mechanism of miR-30a and miR-17.