Persistent and improved functional gain in mdx dystrophic mice after treatment with L -arginine and deflazacort Jonathan D. Archer, Cinthya C. Vargas and Judy E. Anderson 1 Department of Human Anatomy and Cell Science, Faculty of Medicine, University of Manitoba, Winnipeg, Canada 1 Correspondence: Faculty of Medicine, University of Manitoba, 730 William Ave., Winnipeg, MB R3E 0W3, Canada. E-mail: janders@ms.umanitoba.ca <h3>SPECIFIC AIMS</h3> Experiments were designed to test the hypothesis that combined treatment with deflazacort and L -arginine would mitigate dystrophic fiber injury induced by 24 h of voluntary exercise, increase myogenic cell proliferation, and change the progressive loss of function in mdx mouse dystrophy. <h3>PRINCIPAL FINDINGS</h3> Remarkably, in addition to promoting proliferation and preventing exercise-induced damage and regeneration in the short term, functional gain at the end of treatment not only persisted, but was increased 3 months after treatment. We used a physiologic muscle injury, 24 h of voluntary exercise, to induce a repair response in mdx mouse dystrophic muscle after 17 days of a double-blind treatment protocol [placebo, deflazacort, deflazacort plus L -arginine (NOS substrate) or deflazacort plus L -NAME (NOS inhibitor)]. <h3>1. Acute effects on muscle injury</h3> In a pilot study on placebo-treated mice (measured as
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Persistent and improved functional gain in mdx dystrophic mice after treatment with L-arginine and deflazacort
Archer, Jonathan D.; Vargas, Cinthya C.; Anderson, Judy E.
Follow The FASEB Journal
, Volume 20 (6): 738
Fed of American Socs for Experimental Biology – Apr 1, 2006
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