Peptide OM-LV20 demonstrates neuroprotective effects by attenuating mitochondria-mediated neuronal apoptosis and dysfunction in mice with traumatic brain injury.

Traumatic brain injury (TBI) remains a major public health challenge worldwide, particularly among individuals under 45 years of age, resulting in profound physical disability, neuropsychiatric impairment, and socioeconomic burden. Existing therapeutic strategies offer limited efficacy, underscoring the urgent need for novel treatment modalities. This study evaluated the neuroprotective potential of OM-LV20, an amphibian-derived bioactive peptide, in a murine model of TBI. Intraperitoneal administration of OM-LV20 following controlled cortical impact significantly reduced brain water content and attenuated neurological and cognitive deficits. Histological analysis, TUNEL staining, and ultrastructural assessments revealed suppression of neuronal degeneration and mitigation of mitochondrial dysfunction. Transcriptomic profiling, together with RT-qPCR and western blot analyses, revealed modulation of the expression of apoptosis-related genes and proteins, indicating a robust anti-apoptotic effect mediated through mitochondrial pathways. Additionally, OM-LV20 exhibited efficient permeability across the blood-brain barrier. These findings indicate that OM-LV20 exerted strong neuroprotective activity through targeted suppression of mitochondria-centered neuronal apoptosis, supporting its potential utility in ameliorating neurological dysfunction post-TBI. The diverse mechanistic actions identified for OM-LV20 provide a novel therapeutic avenue with considerable promise for enhancing neurological recovery in individuals with TBI.