The Effects of Antioxidants and Pulsed Magnetic Fields on Slow and Fast Skeletal Muscle Atrophy Induced by Streptozotocin: A Preclinical Study

Background and Objectives. Skeletal muscle atrophy, a condition characterized by decreased muscle mass and contractility, is commonly observed in various pathological states, including prolonged inactivity, malnutrition, sarcopenia, and type 1 diabetes mellitus (T1DM). We aimed to investigate the potential therapeutic effects of pterostilbene (PTS), resveratrol (RSV), pulsed magnetic field (PMF), and their combinations on the streptozotocin- (STZ-) induced atrophy of slow- and fast-twitch skeletal muscles in rats. Material and Methods. Biomechanical analyses were utilized to examine the contractions of soleus and extensor digitorum longus (EDL) muscles, while muscle morphology was evaluated using hematoxylin-eosin staining. Immunohistochemical methods were employed to assess atrophy-related markers, including FBXO32, TRIM63, and FoxO3a. The levels of key proteins, such as pAkt, mTOR, FoxO3a, MSTN, CAPN3, TNF-α, NF-κB, MyHC IIb, MyLC 3, and GLUT4, in both skeletal muscle tissue and serum insulin levels were determined using ELISA. Total protein concentration was measured using the Bradford protein assay, and relative gene expressions of FBXO32, TRIM63, FoxO3a, 4E-BP1, p70S6K, TRIM72, and UbC were analyzed by real-time PCR. Results. Our findings suggest that antioxidants and PMF may alleviate impaired protein synthesis and degradation pathways in skeletal muscle atrophy. PTS showed a positive effect on the anabolic pathway, while RSV and PMF demonstrated potential for ameliorating the catabolic pathway. Notably, the combination therapy of antioxidants and PMF exhibited a stronger ameliorative effect on skeletal muscle atrophy than either intervention alone. Conclusion. The present results highlight the benefits of employing a multimodal approach, involving both antioxidant and PMF therapy, for the management of muscle-wasting conditions. These treatments may have potential therapeutic implications for skeletal muscle atrophy.