Abstract: Objective: To investigate the repair effect of cannabinoid (WIN55212-2) on the myelin sheath of the demyelination model mice induced by cuprizone, and to elucidate its possible mechanism. Methods: A total of 95 C57BL/6 mice were randomly divided into blank control group, model group (0.2% cuprizone for 6 weeks),DMSO group (intraperitoneally injected with the same amount of DMSO mixture from the 3rd week of feeding 0.2% cuprizone) and treatment group (intraperitoneally injected with 1 mg·kg^-1 WIN55212-2 from the 3rd week of feeding 0.2% cuprizone). The myelin sheath tissue of the mice was stained by Black-gold Ⅱ staining technique, and its histomorphology was observed. The expression levels of juxtanodin(JN),myelin basic protein(MBP) and Nkx2.2 proteins in mouse brain tissue were detected by Western blotting method. Results: The results of Black-goldⅡstaining showed that the corpus callosum of the brain of the mice in blank control group had significant coloration, while the corpus callosum of the mice in model group showed less coloration.Compared with blank control group, the expression levels of JN and MBP proteins in brain tissue of the mice in model group were significantly decreased(P<0.05).Compared with model group and DMSO group, the expression level of JN and Nkx2.2 proteins in brain tissue of the mice in treatment group were significantly increased(P<0.05 or P<0.01). Conclusion: Cannabinoid may promote the JN expression in brain tissue of the cuprizone-induced demyelinating model mice through the transcription factor Nkx2.2, and further promote the remyelination and repair.

Key words: cannabinoid, cuprizone, juxtanodin, transcription factor Nkx2.2, demyelination