Abstract
Background and Study Aims Spinal cord injury (SCI) is one of the most complicated pathologies that affect active
young males. miR-21 primarily regulates several cellular processes. We aimed to elucidate
the regulatory role of miR-21 and test methylprednisolone as a disease-modifying agent
on experimental SCI tissues.
Methods A total of 36 8- to 10-week-old adult female Sprague-Dawley rats weighing 250 to
300 g were used. Animals were randomly divided into six groups. Except for groups
1 and 4, the spinal trauma model was applied to all animal groups using the clipping
method. In groups 3 and 6, methylprednisolone was given. For real-time polymerase
chain reaction (PCR) investigations, rats in groups 1, 2, and 3 were reoperated on
after the first postoperative day, whereas those in groups 4, 5, and 6 were reoperated
on after postoperative day 7 and spinal cord samples from the laminectomy area were
removed for gene expression analysis. Relative gene expression of miR-21, Gfap, Vim, Stat3, Faslg, Pten, Bax, Bcl2, Cox2, and Il6 were determined with quantitative reverse transcription (qRT) PCR.
Results In group 3, the miR-21 expression significantly increased compared with groups 1
and 2. When compared with group 3, a decrease in miR-21 expression was observed in
group 6 (p < 0.05). When compared with group 4, group 6 had lower levels of Gfap, Pten, Stat3, and Bax (p < 0.05).
Conclusions miR-21 supports the beneficial aspects of the body's healing mechanisms following
SCI. In the acute phase, the use of methylprednisolone increases miR-21 expression
in the early period of trauma. Methylprednisolone increases some astrogliosis and
inflammation biomarkers' levels; however, it did not affect the apoptotic biomarkers.
Keywords
spinal cord injury - miR-21 - methylprednisolone - real-time PCR
