Abstract
Carbon tetrachloride (CCl(4)) is a toxic compound that causes severe oxidative stress and inflammation in skeletal muscles, resulting in structural damage, mitochondrial dysfunction, and impaired contractile function. While CD45 and melatonin (MLT) are implicated in immune modulation and antioxidative defense, their precise roles in mitigating CCl(4)-induced muscle damage remain incompletely understood, warranting further investigation. This study used 24 Wistar rats divided into four groups to evaluate the effects of MLT on CCl(4)-induced muscle inflammation. The first group was used as a control group, the second received only MLT (50 mg/kg), and the third group received CCl(4), while the fourth group received MLT (50 mg/kg) and CCl(4). Muscle tissues, obtained 24 h after the commencement of the experiment, were analyzed using biochemical assays for inflammatory markers, histological staining, and immunohistochemistry to assess structural and cellular changes. CCl(4) exposure significantly increased NF-κB activity, nitric oxide levels, iNOS expression, and CD45-positive immune cell infiltration in skeletal muscles, indicating heightened inflammation and oxidative stress. Pretreatment with MLT markedly reduced these inflammatory markers, restoring damaged tissue and diminishing immune cell infiltration. Histological analyses confirmed reduced inflammatory cell presence and tissue damage in MLT-treated animals, highlighting its protective effects. Melatonin demonstrates significant protective effects against CCl(4)-induced skeletal muscle damage by reducing inflammation, oxidative stress, and immune cell infiltration, highlighting its potential as a therapeutic agent.