| Autor: |
Nagata I; Department of Rehabilitation Sciences, Kobe University Graduate School of Health Sciences, Kobe, Japan., Kawashima M; Department of Rehabilitation Sciences, Kobe University Graduate School of Health Sciences, Kobe, Japan.; Department of Health and Sports Science, Kawasaki University of Medical Welfare, Kurashiki, Japan., Miyazaki A; Department of Rehabilitation Sciences, Kobe University Graduate School of Health Sciences, Kobe, Japan., Miyoshi M; Department of Biophysics, Kobe University Graduate School of Health Sciences, Kobe, Japan., Sakuraya T; Department of Rehabilitation Sciences, Kobe University Graduate School of Health Sciences, Kobe, Japan.; Department of Oral Anatomy, Asahi University School of Dentistry, Gifu, Japan., Sonomura T; Department of Oral Anatomy, Asahi University School of Dentistry, Gifu, Japan., Oyanagi E; Department of Health and Sports Science, Kawasaki University of Medical Welfare, Kurashiki, Japan., Yano H; Department of Health and Sports Science, Kawasaki University of Medical Welfare, Kurashiki, Japan.; Graduate School of Health Science and Technology, Kawasaki University of Medical Welfare, Kurashiki, Japan., Arakawa T; Department of Rehabilitation Sciences, Kobe University Graduate School of Health Sciences, Kobe, Japan. |
| Abstrakt: |
Growing evidence from animal experiments suggests that icing after skeletal muscle injury is harmful to muscle regeneration. However, these previous experimental models yielded massive necrotic myofibers, whereas muscle injury with necrosis in a small myofiber fraction (<10%) frequently occurs in human sports activities. Although macrophages play a proreparative role during muscle regeneration, they exert a cytotoxic effect on muscle cells through an inducible nitric oxide synthase (iNOS)-mediated mechanism. In this study, we established an animal injury model with necrosis limited to a small myofiber fraction and investigated the effect of icing on muscle regeneration with a focus on macrophage-related events. Icing after muscle injury of this model resulted in an enlarged size of regenerating myofibers compared with those in untreated animals. During the regenerative process, icing attenuated the accumulation of iNOS-expressing macrophages, suppressed iNOS expression in the whole damaged muscle, and limited the expansion of the injured myofiber area. In addition, icing increased the ratio of M2 macrophages within the injured site at an earlier time point than that in untreated animals. Following these phenomena in icing-treated muscle regeneration, an early accumulation of activated satellite cells within the damaged/regenerating area occurred. The expression level of myogenic regulatory factors, such as MyoD and myogenin, was not affected by icing. Taken together, our results suggest that icing after muscle injury with necrosis limited to a small fraction of myofibers facilitates muscle regeneration by attenuating iNOS-expressing macrophage invasion, limiting muscle damage expansion, and accelerating the accumulation of myogenic cells which form regenerating myofibers. |
