Aim: 

Experimental autoimmune encephalomyelitis (EAE) is an animal model for human multiple sclerosis (MS). The present study was aimed at evaluating the expression of three metallothionein isoforms (MT-1, MT-2 and MT-3) and the level of oxidative stress in brain during EAE onset and progression following murine mesenchymal stem cell (MSCs) treatment.

Methods: 

C57BL/6J mice were immunized with MOG35-55 peptide. At the disease onset, mice were injected i.v. with MSCs; control mice received an equal volume of PBS.In brain, transcription of the three MTs was assessed by 'real-time' quantitative PCR. Moreover, the activity of two antioxidant enzymes catalase (CAT) and superoxide dismutase (SOD) was determined spectrophotometrically.

Results: 

Expression of all MT isoforms was increased in EAE mice with respect to controls, already at day 11 from the onset of the disease and even more at day 40. In mice treated with MSCs, up-regulation of MTs was partially reversed. Changes in CAT and SOD activity parallel those observed in MT expressions.

Conclusion: 

The results demonstrate that EAE progression is clearly associated with development of oxidative stress conditions in the brain. Treatment with MSCs significantly reduces both MT up-regulation and increased antioxidant enzyme activities accompanying the progression of the disease.