Investigation of the Anti-Inflammatory and Antioxidant Effects of Magnesium Malate in a Model of LPS-Induced Acute Endotoxemia

Background and Aim: Sepsis-associated skeletal muscle injury involves interactions among inflammation, oxidative stress, and disrupted trace element homeostasis. This study investigated the effects of magnesium malate (MgM) on these processes in a rat model of LPS-induced acute endotoxemia. Materials and Methods: Twenty-one male Sprague–Dawley rats were assigned to three groups (n = 7): Control, LPS (8 mg/kg, i.p.), and LPS + MgM (8 mg/kg LPS, followed by 200 mg/kg MgM, i.p., 1 h later). Six hours after LPS administration, serum TNF-α, IL-1β, IL-10, procalcitonin, and presepsin, as well as muscle IL-6, were measured by ELISA. Muscle Cu, Fe, and Zn levels were determined by ICP-OES. Histopathological and electrophysiological assessments were performed, and tissue CAT, GSH, and MDA levels were measured. Results: LPS significantly increased serum TNF-α, IL-1β, IL-10, and presepsin, as well as muscle IL-6 and Fe levels (p < 0.05–p < 0.01). It also caused severe muscle fiber degeneration and interstitial edema, with moderate inflammation (p < 0.001). MgM significantly reduced histopathological scores for degeneration, edema, and inflammation (p < 0.05), attenuated the reduction in motor unit potential (MUP) amplitude (p < 0.05), and decreased muscle CAT and MDA levels (p < 0.05). Conclusions: MgM attenuated skeletal muscle damage and inflammatory cell infiltration while partially preserving electrophysiological function in acute endotoxemia. It also affected some oxidative stress-related parameters. However, its effects on inflammatory markers and trace element levels were limited, with most parameters remaining unchanged. Further studies involving different doses, treatment protocols, and longer follow-up periods are needed to clarify the therapeutic potential of MgM in acute endotoxemia-associated muscle injury.