scholarly journals REHABILITATION THERAPY WITH INSULIN-LIKE GROWTH FACTOR AFTER ACUTE SKELETAL MUSCLE INJURY

2021 ◽  
Vol 27 (3) ◽  
pp. 295-298
Author(s):  
Qing Wang ◽  
Fen Wang
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Muscle Injury ◽  
Control Group ◽  
Protective Film ◽  
Insulin Like Growth Factor ◽  
Muscle Injuries ◽  
Level Of Evidence ◽  
Skeletal Muscle Injury ◽  
Experimental Group

ABSTRACT Introduction Skeletal muscle injuries account for 10% to 50% of treadmill sports injuries. Insulin-like growth factor (IGF) is a family of polypeptides with both insulin-like anabolic and growth-promoting effects. Sports play a vital role in the recovery of skeletal muscle injuries. Objective The paper analyzes the ability of insulin-like growth factor 1 (IGF-1) to repair skeletal muscle injury caused by treadmill exercise. Method We injected drugs under the wound after exercise-induced injury in rats. The control group was injected with saline, and the experimental group was injected with an insulin-like growth factor. We conduct histological and electron microscopic structural analysis of rats, Results: After an injury, the experimental group formed a basal lamina protective film earlier than the control group, activated myoblasts, formed myofilaments, formed myotubes, and fused into muscle fibers earlier than the control group. The healing quality was also better. The experimental group was endogenous. The mRNA content of sex IGF-1 and IGF-2 both increased earlier than the control group. Conclusion Local injection of exogenous insulin-like growth factor-1 can stimulate the proliferation of myoblasts and accelerate the post-traumatic repair process of skeletal muscle caused by treadmill sports. Level of evidence II; Therapeutic studies - investigation of treatment results.

scholarly journals Macrophages recruited via CCR2 produce insulin‐like growth factor‐1 to repair acute skeletal muscle injury

2010 ◽  
Vol 25 (1) ◽  
pp. 358-369 ◽  
Author(s):  
Haiyan Lu ◽  
Danping Huang ◽  
Noah Saederup ◽  
Israel F. Charo ◽  
Richard M. Ransohoff ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Muscle Injury ◽  
Insulin Like Growth Factor ◽  
Skeletal Muscle Injury

scholarly journals EFFECTS OF CONTUSION AND EXHAUSTIVE EXERCISE ON MG53, PTRF IN SKELETAL MUSCLE OF RATS

2019 ◽  
Vol 25 (6) ◽  
pp. 455-459
Author(s):  
Tongbin Pan ◽  
Xinwei Tong ◽  
Leilei Ye ◽  
Mengjin Ji ◽  
Jianjian Jiao
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Muscle Injury ◽  
Exhaustive Exercise ◽  
Control Group ◽  
Repair Mechanism ◽  
Level Of Evidence ◽  
Skeletal Muscle Injury ◽  
Results Of Treatment ◽  
Significant Difference

ABSTRACT Objectives To study the effects of contusion and exhaustive exercise on gene expression of MG53, PTRF, Pax7 and β-catenin in skeletal muscle of rats, and reveal the repair mechanism of skeletal muscle injury. Methods Forty-two male Wistar rats were randomly divided into 7 groups, with 6 rats in each group. All groups were euthanized at different time points after exhaustive exercise and contusion, respectively, while the control group was euthanized in resting state. The right gastrocnemius muscles were measured for mRNAs of MG53, PTRF, Pax7 and β-catenin by real time PCR. Results MG53 mRNA and PTRF mRNA of skeletal muscle in groups immediately after exhaustive exercise and after contusion increased significantly (p<0.05), while the two indices decreased constantly at 24 and 48 hours after injury with a similar change trend. Compared with the control group, Pax7 mRNA of skeletal muscle as a marker showed no significant difference in exhaustive exercise groups, but decreased at 48 hours after contusion (p<0.05). β-catenin mRNA of skeletal muscle down-regulated significantly over 24 hours after injury, then activated with an increased value at 48 hours after contusion (p<0.05). As a whole, the variations in the above indices in the contusion groups covered a wider range than in the exhaustive exercise groups. Conclusion The cytomembrane repair mechanism of MG53 and PTRF began immediately after the end of exhaustive exercise and contusion. Activation of Pax7 as the satellite cell marker took longer, and Wnt/β-catenin pathway showed first a decrease and then an increase resulting from the time-dependent gene expression during the repair of skeletal muscle injury. Level of evidence III, Therapeutic studies investigating the results of treatment.

scholarly journals A Histoarchitectural Approach to Skeletal Muscle Injury: Searching for a Common Nomenclature

2020 ◽  
Vol 8 (3) ◽  
pp. 232596712090909 ◽  
Author(s):  
◽  
Ramon Balius ◽  
Marc Blasi ◽  
Carles Pedret ◽  
Xavier Alomar ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Connective Tissue ◽  
Muscle Injury ◽  
Muscle Injuries ◽  
Macroscopic Anatomy ◽  
Skeletal Muscle Injury ◽  
Tissue Structures ◽  
Definition Of

In recent years, different classifications for muscle injuries have been proposed based on the topographic location of the injury within the bone-tendon-muscle chain. We hereby propose that in addition to the topographic classification of muscle injuries, a histoarchitectonic (description of the damage to connective tissue structures) definition of the injury be included within the nomenclature. Thus, the nomenclature should focus not only on the macroscopic anatomy but also on the histoarchitectonic features of the injury.

scholarly journals Mitochondria-Cytokine Crosstalk Following Skeletal Muscle Injury and Disuse: A Mini-Review

2021 ◽  
Author(s):  
Anita E. Qualls ◽  
W. Michael Southern ◽  
Jarrod A. Call
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Function ◽  
Muscle Injury ◽  
Muscle Injuries ◽  
Monocyte Chemoattractant Protein 1 ◽  
Skeletal Muscle Injury ◽  
Atp Production ◽  
Bona Fide ◽  
Sense And Respond ◽  
And Function

Skeletal muscle mitochondria are highly adaptable, highly dynamic organelles that maintain the functional integrity of the muscle fiber by providing ATP for contraction and cellular homeostasis (e.g., Na+/K+ ATPase). Emerging as early modulators of inflammation, mitochondria sense and respond to cellular stress. Mitochondria communicate with the environment, in part, by release of physical signals called mitochondrial-derived damage-associated molecular patterns (mito-DAMPs) and deviation from routine function (e.g. reduced ATP production, Ca2+ overload). When skeletal muscle is compromised, mitochondria contribute to an acute inflammatory response necessary for myofibril regeneration; however, exhaustive signaling associated with altered or reduced mitochondrial function can be detrimental to muscle outcomes. Here we describe changes in mitochondrial content, structure, and function following skeletal muscle injury and disuse and highlight the influence of mitochondrial-cytokine crosstalk on muscle regeneration and recovery. While the appropriate therapeutic modulation following muscle stressors remains unknown, retrospective gene expression analysis reveal interleukin-6 (IL-6), interleukin-1b (IL-1b), chemokine C-X-C motif ligand 1 (CXCL1), and monocyte chemoattractant protein 1 (MCP-1) are significantly upregulated following three unique muscle injuries. These cytokines modulate mitochondrial function and execute bona fide pleiotropic roles that can aid functional recovery of muscle; however, when aberrant, chronically disrupt healing partly by exacerbating mitochondrial dysfunction. Multidisciplinary efforts to delineate the opposing regulatory roles of inflammatory cytokines in the muscle-mitochondrial environment are required to modulate regenerative behavior following skeletal muscle injury or disuse. Future therapeutic directions to consider include quenching or limited release of mito-DAMPs and cytokines present in cytosol or circulation.

scholarly journals Human Umbilical Cord Mesenchymal Stem Cells Extricate Bupivacaine-Impaired Skeletal Muscle Function via Mitigating Neutrophil-Mediated Acute Inflammation and Protecting against Fibrosis

2019 ◽  
Vol 20 (17) ◽  
pp. 4312 ◽  
Author(s):  
Wen-Hong Su ◽  
Ching-Jen Wang ◽  
Hung-Chun Fu ◽  
Chien-Ming Sheng ◽  
Ching-Chin Tsai ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Growth Factor ◽  
Umbilical Cord ◽  
Muscle Injury ◽  
Acute Inflammation ◽  
Transforming Growth Factor ◽  
Skeletal Muscle Injury ◽  
Tgf Β1

Skeletal muscle injury presents a challenging traumatological dilemma, and current therapeutic options remain mediocre. This study was designed to delineate if engraftment of mesenchymal stem cells derived from umbilical cord Wharton’s jelly (uMSCs) could aid in skeletal muscle healing and persuasive molecular mechanisms. We established a skeletal muscle injury model by injection of myotoxin bupivacaine (BPVC) into quadriceps muscles of C57BL/6 mice. Post BPVC injection, neutrophils, the first host defensive line, rapidly invaded injured muscle and induced acute inflammation. Engrafted uMSCs effectively abolished neutrophil infiltration and activation, and diminished neutrophil chemotaxis, including Complement component 5a (C5a), Keratinocyte chemoattractant (KC), Macrophage inflammatory protein (MIP)-2, LPS-induced CXC chemokine (LIX), Fractalkine, Leukotriene B4 (LTB4), and Interferon-γ, as determined using a Quantibody Mouse Cytokine Array assay. Subsequently, uMSCs noticeably prevented BPVC-accelerated collagen deposition and fibrosis, measured by Masson’s trichrome staining. Remarkably, uMSCs attenuated BPVC-induced Transforming growth factor (TGF)-β1 expression, a master regulator of fibrosis. Engrafted uMSCs attenuated TGF-β1 transmitting through interrupting the canonical Sma- And Mad-Related Protein (Smad)2/3 dependent pathway and noncanonical Smad-independent Transforming growth factor beta-activated kinase (TAK)-1/p38 mitogen-activated protein kinases signaling. The uMSCs abrogated TGF-β1-induced fibrosis by reducing extracellular matrix components including fibronectin-1, collagen (COL) 1A1, and COL10A1. Most importantly, uMSCs modestly extricated BPVC-impaired gait functions, determined using CatWalk™ XT gait analysis. This work provides several innovative insights into and molecular bases for employing uMSCs to execute therapeutic potential through the elimination of neutrophil-mediated acute inflammation toward protecting against fibrosis, thereby rescuing functional impairments post injury.

A Histological Study on the Effect of Dextrose Prolotherapy on Skeletal Muscle Injury in Adult Male Albino Rats

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Eman diaa eldeen ◽  
Azza Salah El Din Soliman ◽  
Rania Ahmed Salah El Din ◽  
George Fayek Barsoum Hanna ◽  
Shereen Adel Saad
Keyword(s):  
Skeletal Muscle ◽  
Adult Male ◽  
Muscle Injury ◽  
Treated Group ◽  
Untreated Group ◽  
Control Group ◽  
Albino Rats ◽  
Muscle Injuries ◽  
Group Iii ◽  
Group Ii

Abstract Background Skeletal muscle injuries are one of the most common injuries occurring in sport medicine varies from 10% to 55% of all injuries. Phases of muscle injuries includes a series of complex stages including inflammation, regeneration and remodeling. Treatment of the injuries is based on conservative measures as rest, elevation, physical therapy and non steroidal anti-inflammatory medications. Many injection protocols have been proposed for the treatment of muscle lesions as corticosteroid injection. Recently prolotherapy appears to have a safety profile comparable with other injection procedures. Aim of the work The aim of the present work is to determine the efficacy of dextrose prolotherapy in treatment of skeletal muscle injury in adult male albino rats. Material and methods Sixty six adult male albino rats were used in the study. They were divided into control (group I) and experimental groups. Control group: rats were left without any intervention. The experimental group was group II that was divided into sham operated group in which skin incision was done in the left hindlimb without injury to gastrocnemius (group II`) and muscle injury group in which transverse cut injury across the midbelly of the gastrocnemius muscle of right hindlimb was done (group II``) and group III that was divided into lidocaine injected group in which skin incision in lefthindlimb was done without injury to gastrocnemius followed by injection of 0.3 ml 1% lidocaine was injected across the muscle (group III`) and muscle injury treated with dextrose prolotherapy group in which a transverse cut injury across the midbelly of gastrocnemius of right hindlimb was done followed by injection of 0.1 ml of dextrose prolotherapy of mixture of 0.1ml of 12.5% dextrose and 0.3 ml of 1% lidocaine (group III``). The animals were received 6 injections of lidocaine and dextrose prolotherapy at 5 days interval (starting from day 0 to day 25). In group II and III, muscle specimens were taken at 5,12 and 28 days and processed for light microscope Results Examination of Group II``A (5 days untreated group) showed intense infiltration of mononucleated inflammatory cells intermingling with dispersed myoblasts and macrophages. Group II`` B (12 days untreated group) showed regenerating myotubes intermingling with mononuclear inflammatory infiltrate and macrophages. Group II``C (28 days untreated group) showed some muscle fibers with peripherally elongated nuclei while others showed centrally vesicular ones. Examination of group III``A (5 day treated group with prolotherapy) showed longitudinal regenerating myofibers with multiple rows of internal vesiculated nuclei. Group III``B (12 days treated group) showed newly formed myofibers with incomplete striations together with well developed newly formed striated longitudinal muscle bundles with peripheral flattened nuclei, group III``C (28 days treated group) showed cross striated muscle fibers with the appearance of elongated vesicular nuclei. Conclusions dextrose prolotherapy was effective in soft tissue healing as it accelerated myoblast proliferation and differentiation

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