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Nagla A. El‑Sherbeeny,Afaf T. Ibrahiem,Howaida S. Ali,Noha E. Farag,Eman A. Toraih,Sawsan A. Zaitone 대한약학회 2020 Archives of Pharmacal Research Vol.43 No.7
This work tested the role of carbamazepine inalleviating alloxan-induced diabetic neuropathy and theenhancement of spinal plasticity. Mice were randomizedinto four groups: normal, control, carbamazepine (25-mg/kg) and carbamazepine (50-mg/kg). Nine weeks after inductionof diabetes, symptoms of neuropathy were confirmedand carbamazepine (or vehicle) was given every other dayfor five weeks. After completing the treatment period, micewere sacrificed and the pathologic features in the spinal cordand the sciatic nerves were determined. The spinal cordswere evaluated for synaptic plasticity (growth associated protein-43, GAP43), microglia cell expression (by CD11b)and astrocyte expression (glial fibrillary acidic protein,GFAP). Further, sciatic nerve expression of Nav1.5 wasmeasured. Results revealed that carbamazepine 50 mg/kgprolonged the withdrawal threshold of von-Frey filamentsand increased the hot plate jumping time. Carbamazepineimproved the histopathologic pictures of the sciatic nervesand spinal cords. Spinal cord of carbamazepine-treatedgroups had enhanced expression of GAP43 but lower contentof CD11b and GFAP. Furthermore, specimens from thesciatic nerve indicated low expression of Nav1.5. In conclusion,this work provided evidence, for the first time, that thepreventive effect of carbamazepine against diabetic neuropathyinvolves correction of spinal neuronal plasticity and gliacell expression.