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      Protective Effects of Resveratrol Supplementation on Contusion Induced Muscle Injury

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          Abstract

          Muscle injuries frequently occur in contact sports events. The current treatment options for soft tissue injuries remain suboptimal and often result in delayed or incomplete recovery of damaged muscles. Resveratrol (RES) is a phenolic phytochemical, well-known for its antioxidant and anti-inflammatory properties. The purpose of this study is to evaluate the potential beneficial effects of RES supplementation on inflammation and regeneration in skeletal muscle after a contusion injury, in comparison to a conventional treatment of nonsteroidal anti-inflammatory drugs (NSAID). After one week of acclimation, forty eight -week-old male ICR mice were randomly divided into the five groups (n=8 per group): 1) normal control (NC), 2) mass-drop injury without any treatment (mass-drop injury, MDI), 3) post-injury NSAID treatment (MDI+ 10mg/kg NSAID), 4) post-injury RES supplementation (MDI+ 25mg/kg/day RES) and 5) post-injury treatment with RES and NSAID (MDI + resveratrol+ NSAID). After muscle contusion injury of the left gastrocnemius muscle, RES or NSAID were orally administered post-injury once a day for 7 days. Results showed that the MDI group had significantly higher serum uric acid (UA), CREA (creatinine), LDH (lactic dehydrogenase) and creatine kinase (CK) than the normal control group. Treatment with resveratrol reduced muscle damage as evidenced by the significantly decreased serum levels of UA, CREA, LDH and CK after contusion-induced muscle injuries in mice. In addition, RES and RES + NSAID groups promoted muscle satellite cell regeneration with increase in desmin protein after injury. Our results suggest that resveratrol combined with NSAID potentially improve muscle recovery and may be a potential candidate for further development as an effective clinical treatment for muscle repair.

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          Most cited references 43

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          Inflammatory processes in muscle injury and repair.

          Modified muscle use or injury can produce a stereotypic inflammatory response in which neutrophils rapidly invade, followed by macrophages. This inflammatory response coincides with muscle repair, regeneration, and growth, which involve activation and proliferation of satellite cells, followed by their terminal differentiation. Recent investigations have begun to explore the relationship between inflammatory cell functions and skeletal muscle injury and repair by using genetically modified animal models, antibody depletions of specific inflammatory cell populations, or expression profiling of inflamed muscle after injury. These studies have contributed to a complex picture in which inflammatory cells promote both injury and repair, through the combined actions of free radicals, growth factors, and chemokines. In this review, recent discoveries concerning the interactions between skeletal muscle and inflammatory cells are presented. New findings clearly show a role for neutrophils in promoting muscle damage soon after muscle injury or modified use. No direct evidence is yet available to show that neutrophils play a beneficial role in muscle repair or regeneration. Macrophages have also been shown capable of promoting muscle damage in vivo and in vitro through the release of free radicals, although other findings indicate that they may also play a role in muscle repair and regeneration through growth factors and cytokine-mediated signaling. However, this role for macrophages in muscle regeneration is still not definitive; other cells present in muscle can also produce the potentially regenerative factors, and it remains to be proven whether macrophage-derived factors are essential for muscle repair or regeneration in vivo. New evidence also shows that muscle cells can release positive and negative regulators of inflammatory cell invasion, and thereby play an active role in modulating the inflammatory process. In particular, muscle-derived nitric oxide can inhibit inflammatory cell invasion of healthy muscle and protect muscle from lysis by inflammatory cells in vivo and in vitro. On the other hand, muscle-derived cytokines can signal for inflammatory cell invasion, at least in vitro. The immediate challenge for advancing our current understanding of the relationships between muscle and inflammatory cells during muscle injury and repair is to place what has been learned in vitro into the complex and dynamic in vivo environment.
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            The NAD(+)-dependent SIRT1 deacetylase translates a metabolic switch into regulatory epigenetics in skeletal muscle stem cells.

            Stem cells undergo a shift in metabolic substrate utilization during specification and/or differentiation, a process that has been termed metabolic reprogramming. Here, we report that during the transition from quiescence to proliferation, skeletal muscle stem cells experience a metabolic switch from fatty acid oxidation to glycolysis. This reprogramming of cellular metabolism decreases intracellular NAD(+) levels and the activity of the histone deacetylase SIRT1, leading to elevated H4K16 acetylation and activation of muscle gene transcription. Selective genetic ablation of the SIRT1 deacetylase domain in skeletal muscle results in increased H4K16 acetylation and deregulated activation of the myogenic program in SCs. Moreover, mice with muscle-specific inactivation of the SIRT1 deacetylase domain display reduced myofiber size, impaired muscle regeneration, and derepression of muscle developmental genes. Overall, these findings reveal how metabolic cues can be mechanistically translated into epigenetic modifications that regulate skeletal muscle stem cell biology.
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              Estrogen receptor analyses. Correlation of biochemical and immunohistochemical methods using monoclonal antireceptor antibodies.

              Attempts at histochemical localization of estrogen receptor with anti-steroid antibody or some fluoresceinated estrogens have given unacceptable sensitivities and specificities when compared with biochemical methods or clinical response. In the present study a monoclonal antibody against estrogen receptor (H222 Sp gamma) was used on cryostat sections of freshly frozen breast tumors with a peroxidase-antiperoxidase immunoperoxidase technique. Biochemical receptor analyses were by dextran-coated charcoal analyses. Tumors from three separate cohorts of patients were studied as follows: population A, 62 primary breast cancers from 1983; population B, 72 primary lesions stored from 1976 to 1983; and population C, 23 patients with metastases, treated with hormonal therapy. Distinct staining was seen in the cell nucleus. A semiquantitative relationship was seen between histochemical score assessment of staining and biochemical assay in each cohort. The sensitivity and specificity using a threshold of 75 for the histochemical score and more than 20 femtomoles/mg of protein for dextran-coated charcoal analyses were as follows: population A, specificity, 89%, and sensitivity, 95%; population B, specificity, 94%, and sensitivity 88%; and for population C, the comparison was with objective clinical response yielding specificity, 89%, and sensitivity, 93%.
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                Author and article information

                Journal
                Int J Med Sci
                Int J Med Sci
                ijms
                International Journal of Medical Sciences
                Ivyspring International Publisher (Sydney )
                1449-1907
                2020
                1 January 2020
                : 17
                : 1
                : 53-62
                Affiliations
                [1 ]Graduate Institute of Sports Science, National Taiwan Sport University, Taoyuan 33301, Taiwan;
                [2 ]Division of Physical Medicine and Rehabilitation, Lo-Hsu Foundation, Inc., Lotung Poh-Ai Hospital, Yilan 26546, Taiwan.
                [3 ]Center for General Education, Taipei Medical University, Taipei 11031, Taiwan.
                Author notes
                ✉ Corresponding author: Nai-Wen Kan, Center for General Education, Taipei Medical University, No. 250, Wuxing Street, Taipei 11031, Taiwan. E-mail: kevinkan@ 123456tmu.edu.tw .

                Competing Interests: The authors have declared that no competing interest exists.

                Article
                ijmsv17p0053
                10.7150/ijms.35977
                6945554
                © The author(s)

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.

                Categories
                Research Paper

                Medicine

                mass-drop injury, regeneration, nsaid, ldh, ck

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