Temporal study following burn injury in young rats is associated with skeletal muscle atrophy, inflammation and altered myogenic regulatory factors

Burn injury (BI) greater than 40 % has been associated with protein catabolism and it is characterized by a hypermetabolic response followed for muscle loss. The purpose of this study was to investigate the temporal effects of extensive experimental BI in the skeletal muscle distant from lesion, through morphological analysis, expression of genes related to muscle atrophy, inflammation and the myogenic regulatory factors. A total of 60 young male wistar rats were distributed into two groups, control (C) and subjected to scald burn injury (SBI). The animals were euthanized 1, 4 and 14 days post-sham or 45 % of the total body surface BI. The medial head of gastrocnemii muscles were submitted to histopathological, morphometric (muscle fibers area and density), MyoD and myogenin immunoexpression, and gene expression for TNF-alpha, iNOS and E3 ubiquitin ligases (MuRF1 and MAFbx). Histopathological findings were consistent with increased amount of connective tissue and inflammatory process. Muscle fiber area of SBI groups was smaller than C and no differences were found in fiber muscle density. TNF-alpha was higher in SBI groups, one and 14 days post-injury; iNOS expression was higher on the first and fourth day post-injury. MuRF-1 was higher on the day four and MAFbx on the day 14. In conclusion, BI causes inflammation, atrophy and myogenesis stimulation in muscle as a result of systemic host response.