Prophylactic Effects of Honokiol on Spinal Cord in Rats

Abstract

OBJECTIVE: To investigate the prophylactic effect of the antioxidative honokiol on neuron and glial cells in the spinal cord after spinal cord injury biochemically and immunohistochemically. STUDY DESIGN: Twenty Wistar Albino rats were categorized as control and SCI groups. At T10-T11 vertebras, a steel rod was dropped from 10 cm to create a spinal cord injury under anesthesia. Spinal cord injury was created by dropping a 15-gram metal weight down the tube. Immediately after the trauma, 20 mg/kg hono-kiol was administered orally for 7 days. At the end of the experiment, blood samples were taken from the animals and analyzed with various biochemical markers. The spinal cord was excised for routine paraffin tissue protocol. Hematoxylin-eosin stain was used for histol-ogical examination, and caspase-3 and PSTAT-3 anti-bodies were used for immunohistochemistry. RESULTS: MDA, GSH, and MPO values in control, spinal cord injury, and spinal cord injury+ honokiol groups were compared. Both MDA and MPO values were increased in the SCI group as compared with the control and SCI+ honokiol groups, and the increase was statistically significant. GSH content was decreased in the SCI group as compared with the control and SCI+ honokiol groups, and the decrease was statistically sig-nificant. In spinal cord injury, degenerative changes in multipolar and bipolar neurons, dilation and thrombosis in the blood vessels, and increased inflammation were observed. Honokiol administration showed a significant increase in chromatin in canalis ependymalis cells and a decrease in degeneration in multipolar and bipolar neurons. Positive PSTAT-3 expression was observed in multipolar neurons in trauma and diffuse glial cells in the anterior horn and blood vessel endothelial cells. Pos-itive PSTAT-3 expression was observed in ependymal cells and solitary dispersed glial cells, weak PSTAT-3 expression in multipolar and bipolar neuron cells in the honokiol group. An increase in caspase-3 expression in multipolar cells and a positive caspase-3 reaction in solitary glial cells were observed in trauma. Negative caspase-3 activity was observed in canalis ependymalis cells and many glial cells in the honokiol group. CONCLUSION: After traumatic spinal cord injury, degenerative, apoptotic changes in neuron and glial cells developed with increased inflammation and thrombosis in blood vessels. Lipid peroxidation induced damage due to the increase in oxidative stress. Honokiol admin-istration stimulated the reduction of oxidative stress, inflammation, and angiogenetic effect in blood vessels. It is thought that it has a positive effect on the stimulation of apoptotic signals in neuron and glial cells in trauma injury.