Biochemical Study on the Role of Muscle-Specific Ubiquitin Ligase Atrogin-1 in Dexamethasone-Induced Muscle Atrophy in Rats

Background: skeletal muscle atrophy is characterized by a loss of muscle mass resulting from an imbalance between protein breakdown and synthesis, which can be triggered by conditions such as starvation, aging, and other factors like immobilization and nerve damage. Characterized by lower muscle fiber cross-sectional area, reduced protein content, and diminished muscle strength, along with heightened fatigability. The primary objective of this research was to investigate the function of muscle-specific ubiquitin ligase atrogin-1 in the context of dexamethasone-induced muscle atrophy using an animal model. Methods: A study was carried out on 30 male albino rats, who were randomly allocated into two identical groups, each consisting of 15 rats, as follows: Group 1 (the control group), and Group 2 (the group treated with Dexmethazone). The animal’s body weight and muscle strength were evaluated. Serum creatine kinase concentration, Muscle tissue reduced glutathione and nitric oxide levels were measured using colorimetric assay. Atrogin 1 in muscle tissue was detected by ELISA. Histopathological examination and immunohistochemistry of caspase 3. Results: The results of dexamethasone treated group when compared with control group revealed significant reduction of body weight, muscle strength, tissue nitric oxide level, in addition to histopathological changes indicative of muscle atrophy, while there was significant increase in tissue atrogin1and serum creatinine kinase level and immunoreactivity of caspase Conclusion: In view of the assessed data, it can be concluded that Dexamethazone induces muscle atrophy in experimental rats is evidenced by modulation in the biochemical indices and muscle histopathological changes.