Peptide OM-LV20 Demonstrates Neuroprotective Effects by Attenuating Mitochondrial-Mediated Neuronal Apoptosis in Traumatic Brain Injury (TBI) Mice

Traumatic brain injury (TBI) is a significant global health concern, particularly affecting individuals under 45 years old, leading to substantial physical, psychosocial, and economic burdens. Current therapeutic approaches for TBI remain inadequate, necessitating the exploration of novel treatment modalities. In this study, we investigated the neuroprotective potential of the amphibian-derived short peptide OM-LV20 in a TBI mouse model. Through brain water content measurement, neurological and behavioral assessments, histological and TUNEL staining, RNA-sequencing, as well as mRNA and protein level analyses via RT-qPCR and western blot assays, we comprehensively evaluated the effects of OM-LV20 treatment administered via intraperitoneal injection post-TBI. Our findings demonstrated that OM-LV20 intervention significantly alleviated brain edema, improved neurological and cognitive function, inhibited neuronal degeneration, and mitigated mitochondrial dysfunction and apoptosis following TBI. Otherwise, OM-LV20 showed efficient permeability to the blood-brain barrier (BBB). This study highlights the neuroprotective role of peptide OM-LV20 in TBI by targeting mitochondria-centered neuronal apoptosis, suggesting its promising therapeutic application in ameliorating neurological dysfunction post-TBI. The multifaceted functions of OM-LV20 uncovered in this study offer a novel potential therapeutic avenue for enhancing neurological recovery in TBI patients.