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

Journal of Neuroscience Research
Mary K GuytonNaren L Banik

Abstract

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 microg/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.

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Citations

May 22, 2013·Neurochemical Research·Supriti SamantarayNaren L Banik
Jul 19, 2013·Journal of Neuropathology and Experimental Neurology·Dorit B HoffmannRichard Fairless
Oct 31, 2012·Journal of Neurochemistry·Arabinda DasNaren L Banik
Feb 4, 2011·Journal of Neuroscience Research·Kenkichi NozakiNaren L Banik
Oct 2, 2015·Neurochemical Research·Xiaomin WeiSufang Yu
Oct 25, 2016·Journal of Neurochemistry·Maria PodbielskaNaren L Banik
Jan 1, 2013·Brain Sciences·Maria PodbielskaEdward L Hogan
Jun 14, 2019·Frontiers in Cellular Neuroscience·Cheng-Hsin Liu, Matthew Neil Rasband

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