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

ABSTRACT: 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

SUBMITTER: Ye CJ 

PROVIDER: S-EPMC12940741 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature