Carbon tetrachloride (CCl₄) 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 CCl₄-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 CCl₄-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 CCl₄, while the fourth group received MLT (50 mg/kg) and CCl₄. 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. CCl₄ 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 CCl₄-induced skeletal muscle damage by reducing inflammation, oxidative stress, and immune cell infiltration, highlighting its potential as a therapeutic agent.

Sarcopenia is an epidemic that has been recognized only recently, presenting a threat to the functional independence and quality of life of the elderly. Sarcopenia is defined as a loss of muscle mass in combination with changes in muscle quality and physical function. Common causes of sarcopenia are the aging process, an imbalance of sex hormones, lack of physical activity or chronic diseases, which is why sarcopenia, apart from the elderly, can also occur in the younger population. Both dimensions of sarcopenia, quantitative, skeletal muscle loss, and qualitative, loss of quality of life and disability, should be considered when creating and designing preventive and therapeutic measures. There are quick and simple tests for the diagnosis of sarcopenia, but they are still not sufficiently recognized and regularly used as part of physiotherapy assessment.

Background/Objectives: Cisplatin (CP) is a platinum-based chemotherapeutic agent associated with neurotoxicity and cognitive impairment. Due to its high metabolic activity and sensitivity to oxidative stress, the hippocampus represents a particularly vulnerable brain structure. The present study evaluated dose-dependent hippocampal alterations following single-dose cisplatin administration in rats using biochemical, histopathological, and morphometric analyses. Methods: Male Wistar rats were divided into four groups (n = 8): control and cisplatin-treated groups receiving single intraperitoneal doses of 8, 9, or 10 mg/kg. Five days after treatment, hippocampal tissue was analyzed for oxidative stress and inflammatory, apoptotic, and morphological changes. Results: Cisplatin administration significantly increased TBARS and AOPP levels, indicating enhanced lipid and protein oxidation. Elevated hippocampal TNF-α, IL-6, and IL-1β levels demonstrated activation of inflammatory pathways, particularly in animals receiving 9 and 10 mg/kg cisplatin. Higher doses additionally increased Bax/Bcl-2 ratio, caspase-3 content, and DNase I/II activity, consistent with enhanced apoptotic signaling. Histopathological examination revealed neuronal degeneration, pyknotic nuclei, pericellular halo formation, and progressive disruption of hippocampal cytoarchitecture, while morphometric analysis demonstrated significant alterations in neuronal nuclear surface area, predominantly in the 10 mg/kg group. Conclusions: These findings demonstrate that acute cisplatin exposure induces oxidative, inflammatory, apoptotic, and structural progressive hippocampal injury with a threshold-like increase in several endpoints at higher cisplatin doses, with 10 mg/kg producing the most pronounced neurotoxic effects.