Neuroprotective effect of L-deprenyl on the expression level of the Mst۱ gene and inhibition of apoptosis in rat-model spinal cord injury

Objective(s): After primary tissue damage as a result of spinal cord injury (SCI), there is a period of secondary damage, which includes several cellular and inflammatory biochemical cascades. As a novel pro-apoptotic kinase, Mst۱ (serine/threonine kinase ۴) promotes programmed cell death in an inflammatory disease model. This study aimed to evaluate Mst۱ gene expression levels in rats with spinal cord injury treated with L- deprenyl. Materials and Methods: The rats were divided into control (contusion), laminectomy, sham-operated (contused rats received ۱ ml normal saline intraperitoneal), and treatment (contused rats received ۵ mg/kg of L-deprenyl intraperitoneal; once a day for ۷ days). The BBB (Basso, Beattie, and Bresnahan) scales were performed to assess motor function following SCI. Rats were sacrificed ۲۸ days after SCI and the spinal cord lesion area was removed. Apoptosis and cavity formation in the spinal cord were determined by H&E staining and TUNEL assay, respectively. The mRNA levels of the Mst۱, Nrf۲, Bcl-۲, and PGC۱α genes were analyzed using real-time quantitative PCR.Results: The results showed significant improvement in motor function in the L- deprenyl group compared with the untreated group. Histological analysis showed a significant reduction in the number of tunnel-positive cells after injection of L-deprenyl, as well as a decrease in the volume of the cavity. In addition, L-deprenyl treatment increased the expression of the Nrf۲, Bcl-۲, and PGC۱α genes, while reducing the expression of the Mst۱ gene in the spinal nerves. Conclusion: These results suggest that L-deprenyl is a promising treatment for spinal cord injury.

کلیدواژه ها:

Apoptosis ، Bcl-۲ ، Contusion ، L-deprenyl ، Mst۱ ، Nrf۲ ، Selegiline