Neuroprotective potential of asprosin in traumatic brain ınjury: Histopathological and biochemical insights from an...

Traumatic brain injury (TBI) remains a leading cause of morbidity and mortality, yet pharmacological neuroprotection is still an unmet need. Asprosin, a recently identified fasting-induced adipokine, has been implicated in oxidative stress modulation, apoptosis, and metabolic regulation. This study aimed to investigate the neuroprotective role of asprosin in an experimental rat model of TBI.

Thirty-two male Wistar rats were randomized into four groups: Control, Trauma, Trauma+Asprosin, and Asprosin. Moderate head trauma was induced using a validated closed-head injury model. Asprosin (10 µg/kg, intraperitoneal) was administered immediately and 12 h post-trauma. Brain tissues were examined histopathologically (cresyl violet staining) and biochemically for oxidative stress and apoptotic markers, including Glutathione, total oxidant status, superoxide dismutase, Catalase, Malondialdehyde, glutathione peroxidase, nitric oxide, total antioxidant status, asprosin, and caspase-3.

Histopathological evaluation revealed pronounced neuronal degeneration, vacuolization, and darkly stained nuclei in the Trauma and Trauma+Asprosin groups, whereas the control and asprosin-only groups preserved normal cortical and hippocampal architecture. Biochemically, no significant differences were observed among groups for oxidative stress parameters; however, caspase-3 levels were significantly higher in the Asprosin group compared to controls (P = 0.02). These findings suggest that while asprosin modulates apoptosis-related pathways, its direct protective effect against trauma-induced neuronal damage remains inconclusive.

This study provides the first experimental evidence linking asprosin to TBI. Although asprosin demonstrated potential interactions with oxidative and apoptotic processes, its role as a neuroprotective agent requires further validation with larger cohorts, varied dosing regimens, and molecular analyses.