6533b857fe1ef96bd12b3c49

RESEARCH PRODUCT

Prednisolone decreases exercise-induced acid hydrolase response in mouse skeletal muscle.

Veikko VihkoA. SalminenM. Kihlström

subject

Malemedicine.medical_specialtyNecrosisPhysiologymedicine.drug_classPrednisolonePhysical ExertionPhysical exerciseInflammationMice Inbred StrainsBiologyMiceMuscular DiseasesPhysiology (medical)Internal medicinemedicineAnimalsRegenerationOrthopedics and Sports MedicineExertionArylsulfatasesGlucuronidaseMyositisMusclesPublic Health Environmental and Occupational HealthSkeletal muscleGeneral Medicinemedicine.anatomical_structureEndocrinologyGlucoseDepression ChemicalPrednisolonebiology.proteinExercise TestCorticosteroidmedicine.symptomSulfatasesAcid hydrolasemedicine.drug

description

Male NMRI-mice were subjected to exhaustive treadmill exercise. 3 and 6 days after the exertion, quadriceps femoris muscles were examined histologically and analyzed for acid hydrolases in order to follow the degree and progress of injuries. Prednisolone (PRED), an anti-inflammatory corticosteroid, was given to some of the animals in order to modify the exercise response. The PRED administration began 14 h before exercise and continued until the end of the experiment (6 days). The doses were 25 and 50 mg . kg-1 i.p. twice a day. The activities of both arylsulphatase and beta-glucuronidase increased significantly in the exercise control group after 3 and 6 days. The increase in activity correlated with fibre necrosis and an abundant infiltration of inflammatory cells, and was greatest after 3 days. After 6 days the inflammatory response decreased and regenerating muscle fibres were seen. PRED decreased the exercise-induced acid hydrolase response. The decrease was most prominent after 3 days with PRED 50 mg . kg-1 . day-1. PRED also diminished degeneration and inflammation. The results suggest that the decrease in acid hydrolase activities was due to a lesser infiltration of inflammatory cells to the injured area.

10.1007/bf00964690https://pubmed.ncbi.nlm.nih.gov/6542502