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Excessive ROS can induce lipid peroxidation of fatty acids localized near mitochondria, generating reactive peroxides that exert lipotoxic effects on mitochondrial DNA (mtDNA), RNA, and proteins, thereby impairing mitochondrial function ( During lesion progression, activated microglia phagocytose iron released from degenerating oligodendrocytes, a process that may further amplify oxidative tissue damage ( Inflammation and OS are thus tightly interconnected processes in MS, forming a mutually reinforcing and self-perpetuating pathological cycle

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Anesthetized female C57/BL/6 J mice were injected intravenously with saline or glucose (0.125, 0.35 or 0.75 g/kg) with or without simultaneous administration of synthetic tirzepatide (3 nmol/kg)