Neuroprotection unveiled: melatonin mitigates apoptotic pathways in traumatic brain injury.

Objective: This study investigated the neuroprotective effects of melatonin in mice subjected to traumatic brain injury (TBI), focusing on caspase-dependent apoptotic signaling pathways. Materials and methods: A total of 21 mice were divided into three groups: control, trauma (TBI), and trauma + melatonin (TBI + M). TBI was induced in the TBI and TBI + M groups via a free-fall impact on the frontal lobes. A single dose of 10 mg/kg of melatonin was intraperitoneally administered to the TBI + M group. Brain tissues were collected for histological evaluation and immunohistochemical analysis of apoptotic proteins. Results: The control group showed normal brain morphology, while the trauma group exhibited significant tissue loss and demyelination. The TBI + M group demonstrated reduced demyelination compared to the trauma group. An immunohistochemical analysis revealed increased expression of Bax and decreased expression of Bcl-2 in the trauma group, both of which were mitigated by melatonin treatment. The expression levels of caspase-3 and caspase-9 were elevated in the trauma group, whereas the TBI + M group showed expression levels comparable to the control group. Conclusion: TBI increased apoptotic protein expression, indicating neurodegeneration. The administration of melatonin at 10 mg/kg attenuated TBI-induced apoptosis and demyelination while promoting anti-apoptotic protein expression in the experimental model. These findings suggest a potential therapeutic role for melatonin in the management of TBI.