Effects of delayed NSAID administration after experimental eccentric contraction injury – A cellular and proteomics study

Autor: Laura Bond, Therese R. W. Clauss, Bobbie-Jo M. Webb-Robertson, Amy E. Bryant, Dennis L. Stevens, Carrie D. Nicora, Eva J. Katahira, Thomas L. Fillmore, Michael J. Aldape, Thomas O. Metz, Clifford R. Bayer
Rok vydání: 2017
Předmět:
Proteomics
0301 basic medicine
myalgia
Critical Care and Emergency Medicine
NSAIDs
Muscle Proteins
lcsh:Medicine
Apoptosis
Pharmacology
Pathology and Laboratory Medicine
Biochemistry
Mice
0302 clinical medicine
Tibialis anterior muscle
Morphogenesis
lcsh:Science
skin and connective tissue diseases
Immune Response
Cells
Cultured

Trauma Medicine
Caspase
Analgesics
Multidisciplinary
Cell Death
biology
Reverse Transcriptase Polymerase Chain Reaction
Anti-Inflammatory Agents
Non-Steroidal

Drugs
3. Good health
Phenotype
Caspases
Musculoskeletal injury
Infectious diseases
Female
medicine.symptom
Traumatic Injury
Muscle Regeneration
Muscle Contraction
Research Article
Muscle contraction
medicine.medical_specialty
Secondary infection
Bacterial diseases
Immunology
Pain
Inflammation
Ketorolac Tromethamine
03 medical and health sciences
Signs and Symptoms
Diagnostic Medicine
medicine
Animals
Regeneration
Muscle
Skeletal

Cell Proliferation
Medicine and health sciences
lcsh:R
Biology and Life Sciences
Proteins
Myalgia
Group A streptococcal infection
medicine.disease
Pain management
Surgery
Cytoskeletal Proteins
030104 developmental biology
Musculoskeletal Injury
biology.protein
lcsh:Q
Organism Development
030217 neurology & neurosurgery
Developmental Biology
Zdroj: PLoS ONE, Vol 12, Iss 2, p e0172486 (2017)
PLoS ONE
ISSN: 1932-6203
Popis: Background Acute muscle injuries are exceedingly common and non-steroidal anti-inflammatory drugs (NSAIDs) are widely consumed to reduce the associated inflammation, swelling and pain that peak 1–2 days post-injury. While prophylactic use or early administration of NSAIDs has been shown to delay muscle regeneration and contribute to loss of muscle strength after healing, little is known about the effects of delayed NSAID use. Further, NSAID use following non-penetrating injury has been associated with increased risk and severity of infection, including that due to group A streptococcus, though the mechanisms remain to be elucidated. The present study investigated the effects of delayed NSAID administration on muscle repair and sought mechanisms supporting an injury/NSAID/infection axis. Methods A murine model of eccentric contraction (EC)-induced injury of the tibialis anterior muscle was used to profile the cellular and molecular changes induced by ketorolac tromethamine administered 47 hr post injury. Results NSAID administration inhibited several important muscle regeneration processes and down-regulated multiple cytoprotective proteins known to inhibit the intrinsic pathway of programmed cell death. These activities were associated with increased caspase activity in injured muscles but were independent of any NSAID effect on macrophage influx or phenotype switching. Conclusions These findings provide new molecular evidence supporting the notion that NSAIDs have a direct negative influence on muscle repair after acute strain injury in mice and thus add to renewed concern about the safety and benefits of NSAIDS in both children and adults, in those with progressive loss of muscle mass such as the elderly or patients with cancer or AIDS, and those at risk of secondary infection after trauma or surgery.
Databáze: OpenAIRE