Calpeptin attenuated inflammation, cell death, and axonal damage in animal model of multiple sclerosis

M. Kelly Guyton, Arabinda Das, Supriti Samantaray, Gerald C. Wallace IV, Jonathan T. Butler, Swapan K. Ray, Naren L. Banik

Research output: Contribution to journalArticlepeer-review

41 Scopus citations


Experimental autoimmune encephalomyelitis (EAE) is an animal model for studying multiple sclerosis (MS). Calpain has been implicated in many inflammatory and neurodegenerative events that lead to disability in EAE and MS. Thus, treating EAE animals with calpain inhibitors may block these events and ameliorate disability. To test this hypothesis, acute EAE Lewis rats were treated dose dependently with the calpain inhibitor calpeptin (50-250 μg/kg). Calpain activity, gliosis, loss of myelin, and axonal damage were attenuated by calpeptin therapy, leading to improved clinical scores. Neuronal and oligodendrocyte death were also decreased, with down-regulation of proapoptotic proteins, suggesting that decreases in cell death were due to decreases in the expression or activity of proapoptotic proteins. These results indicate that calpain inhibition may offer a novel therapeutic avenue for treating EAE and MS.

Original languageEnglish (US)
Pages (from-to)2398-2408
Number of pages11
JournalJournal of Neuroscience Research
Issue number11
StatePublished - Aug 15 2010
Externally publishedYes


  • Apoptosis
  • Axonal damage
  • Calpain
  • Calpeptin
  • EAE

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience


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