Conclusions
EA at Zusanli promoted macrophage polarization during the fibrotic process in contused skeletal muscle by decreasing cytokine IFN-γ and increasing IL-4, IL-13, and IFN-α, which contributed to the regeneration of the contused skeletal muscle.
Methods
Masson's trichrome staining and hematoxylin and eosin staining were used to measure the area of fibrotic tissue and determine the number of centrally nucleated muscle fibers respectively. The different immune phenotypes of macrophages were determined by flow cytometry. Then, ELISA was used to analyze the levels of interleukin-4 (IL-4), IL-6, interferon-α (IFN-α) and interferon-γ (IFN-γ) in the injured tissue. Finally, the expression of MyoD in the tissue was detected by quantitative real-time polymerase chain reaction.
Objective
To determine whether EA at Zusanli can contribute to the regeneration of contused skeletal muscle and the molecular mechanism involved.
Results
EA at Zusanli helped regenerate contused skeletal muscle by alleviating fibrosis and increasing the size of the regenerating myofibres in the injured skeletal muscle. EA at Zusanli increased the number of M2 macrophages and decreased the number of M1 macrophages in contused skeletal muscle. EA at Zusanli decreased the level of cytokine IFN-γ and increased the levels of IL-4, interleukin-13 (IL-13), and IFN-α, which promoted macrophage polarization during the fibrosis recovery process in the contused skeletal muscle. EA at Zusanli could increase the expression of MyoD in tissues. Conclusions: EA at Zusanli promoted macrophage polarization during the fibrotic process in contused skeletal muscle by decreasing cytokine IFN-γ and increasing IL-4, IL-13, and IFN-α, which contributed to the regeneration of the contused skeletal muscle.