Electrophysiological, functional and histopathological assessments of high dose melatonin on regeneration after blunt sciatic nerve injury.

The aim of this study was to determine the curative effects of high-dose (100 mg/kg) melatonin on peripheral nerve injury. Forty male Wistar albino rats were randomized into four groups as sham, vehicle, melatonin, and ischemia and their right sciatic nerves were exposed. The process was terminated in the sham group. In the other groups, nerve injury was induced by clip compression. The vehicle group was intraperitoneally administered ethanol 0.1 cc (melatonin solvent), while the melatonin group was intraperitoneally administered a single dose of melatonin (100 mg/kg). Following the surgery, sciatic nerve functional index (SFI) was measured using walking track analysis on days 7, 14, and 21, and latency, amplitude, and muscle action potentials (MAP) field values were measured using electroneuromyography (ENMG) on day 21. Histopathologically, edema, axonal degeneration, myelin damage, and inflammatory response were evaluated in all groups. SFI values were noted to be statistically significantly different among the vehicle, melatonin, and ischemia groups, and the melatonin group showed a faster recovery. In the ENMG evaluations, higher amplitude and field values in the melatonin group indicated that melatonin accelerated peripheral nerve recovery. Histopathologically, although fibers with loss of myelin were identified in the melatonin group, the myelin sheath was preserved in general and the axonal structure was noted to be normal. A single injection of high-dose melatonin was found to preserve myelin sheath, prevent axonal loss, and accelerate functional recovery during the nerve regeneration in peripheral nerve injury.

Effects of clotrimazole on experimental spinal cord ischemia/reperfusion injury in rats.

OBJECTIVE: The effect of clotrimazole was examined using a spinal cord ischemia/reperfusion model. METHODS: Twenty albino Wistar rats weighing 234 +/- 12.3 g were used in this study. Rats were anesthetized intraperitoneally with 50 mg/kg ketamine HCl. All animals underwent laparotomy under aseptic conditions. Abdominal aortas of the animals in all but the sham group were exposed. After opening the retroperitoneum, the infrarenal abdominal aorta was clipped for 45 minutes to produce ischemia/reperfusion injury. Polyethylene glycol (PEG, 1 mL) was administrated to the vehicle group. PEG (1 mL) and clotrimazole (30 mg/kg) were administered intraperitoneally in the clotrimazole group. Total laminectomy of T8-T12 was performed on all rats under a microscope. Spinal cords were excised for a length of 2-cm rostrally and 1-cm caudally to the injury site and deep frozen at -76 degrees C for biochemical studies. The levels of malondialdehyde, glutathione-peroxidase, superoxide dismutase, and catalase were measured as an indicator of ischemia level. The most cranial part of the specimens was evaluated morphologically. RESULTS: Treatment with clotrimazole significantly decreased malondialdehyde, glutathione-peroxidase, superoxide dismutase, and catalase levels in comparison with other groups (P = 0.008). Morphologic evaluation revealed that clotrimazole protected the axons and their myelin sheaths from ischemic damage. CONCLUSION: This study showed the neuroprotective effects of clotrimazole on spinal cord ischemia/reperfusion injury.

Effects of clotrimazole on experimental spinal cord injury.

BACKGROUND: We examined a possible neuroprotective effect of clotrimazole on spinal cord clip compression injury. METHODS: Rivlin and Tator's acute extradural clip compression injury (CCI) model was used for producing SCI on 24 albino Wistar rats weighing 180-250 g. All rats were anesthetized with 30 mg/kg ketamine HCl intraperitoneally and were breathing spontaneously without tracheal intubation. Total laminectomy of T8-T12 was performed on all rats under operation microscope, and CCI was performed on all rats (expect those in group 1) with a 50-g closing force aneurysm clip for 1 min. Three hours later, all of the rats were killed with sodium pentobarbital. Spinal cords were excised for a length of 2 cm; 1 cm rostrally and caudally to the injury site and deep frozen at -76 degrees C for biochemical studies. RESULTS: Treatment with clotrimazole decreased MDA levels in rats with SCI with a statistically significant difference. CONCLUSIONS: To our knowledge, this the first study that shows the effects of clotrimazole on spinal cord clip compression injury. Clotrimazole was found to be effective on spinal cord clip compression injury, but further investigations are mandatory.