Issue release date: 12.11.2024
2Serik State Hospital, Department of Neurosurgery, Antalya, Turkey
3Necmettin Erbakan University, Meram School of Medicine, Department of Pathology, Konya, Turkey
4Necmettin Erbakan University, Meram School of Medicine, Department of Biochemistry, Konya, Turkey
5Necmettin Erbakan University, Meram School of Medicine, Department of Public Health, Konya, Turkey DOI : 10.5137/1019-5149.JTN.11749-14.1 AIM: Previous studies have shown that carvedilol has a neuroprotective effect in animal models of brain ischemia and brain oxidative damage in vitro. This study was perfomed to investigate the effect of carvedilol on the secondary damage in experimental spinal cord injury (SCI).
MATERIAL and METHODS: Twenty-four Wistar albino rats were divided into three groups. Group 1 underwent laminectomy alone. Group 2 underwent laminectomy followed by SCI and received carvedilol. Group 3 underwent laminectomy followed by SCI and received no medication. The neurological functions were assessed by Tarlov’s motor scale at the first and 24th hours. Oxidative stress status was assessed by MDA, SOD, MPO, GSH activities. A TUNEL-based apoptosis kit was used for evaluating apoptosis in the spinal cord samples and hematoxylinand eosin-stained specimens were used for light microscopic examination.
RESULTS: Carvedilol reduced apoptosis and regulated oxidant and antioxidant status by increasing SOD and GSH levels and reducing MPO and MDA levels in the spinal tissue homogenate. Neurological examination of rats revealed statistically significant improvement 24 hours after the trauma.
CONCLUSION: Carvedilol has a statistically significant therapeutic effect, especially on functional recovery, and we found that carvedilol reduced secondary damage by inhibiting apoptosis and regulating the oxidant and antioxidant status.
Keywords : Carvedilol, Spinal trauma, Apoptosis, Secondary damage