Browsing by Author "Reeves, Christopher Nicolas"

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    The nitric oxide donor Molsidomine shows therapeutic benefit toward muscle repair after an acute impact injury, in rats.
    (Stellenbosch : Stellenbosch University, 2016-12) Reeves, Christopher Nicolas; Myburgh, Kathryn H.; Smith, Carine; Stellenbosch University. Faculty of Science. Dept. of Physiological Sciences.
    ENGLISH ABSTRACT: Background: Muscle injuries are highly prevalent and arise from a multitude of situations. Trauma to the soft tissue is painful and debilitating and it requires extensive healing that often involves the formation of a fibrotic scar. Current treatments are merely management strategies, such as the RICE principle. Nitric oxide (NO) knock-out models show reduced skeletal muscle regeneration and excessive fibrosis (Filippin et al., 2011 a & b), suggesting therapeutic promise for NO. NO-donation has shown therapeutic promise in mouse models of muscular dystrophy, and therefore, may be beneficial for the treatment of acute muscle injuries. Objective: To clarify the role of treatment-derived NO on muscle trauma, using the NO-donating drug: Molsidomine (MOLS), which has been approved for use in humans. Methods: Using a crush injury model in rats, placebo (PLA) or MOLS treatments were administered immediately and one day after the injury. MPO, MyoD, myogenin, fibronectin and TGF-β1 protein content in the injured tissue homogenates was assessed with Western blots. Collagen deposition at 21 days after injury was assessed using a Masson’s trichrome stain. Results: With MOLS, there was significantly less collagen deposition (p < 0.05) 21 days after injury, which was supported by less TGF-β1 protein (p = 0.01) and less fibronectin protein (p < 0.005) compared to the PLA group at this time point. Additionally, MOLS tended to modulate the amount of MPO and, therefore, the inflammatory response by 33% 5 days after injury. Conclusion: MOLS treatment improves, and potentially hastens, tissue repair after an acute impact injury through the reduction of excessive fibrosis, as well as through enhanced clearance of inflammatory radicals from injured muscle.