Changes in Blood Brain-Derived Neurotrophic Factor (BDNF) Levels in Experimental Animals with Traumatic Brain Injury after Magnesium Sulfate Administration: An Experimental Study

Background: Traumatic brain injury (TBI) results in notable impairments in neurological function and is associated with poor outcomes. Various processes occur at the cellular level, one of which is neuroinflammation. Brain-derived neurotrophic factor (BDNF) is a neurotrophin protein produced by the brain that circulates in plasma post-injury. It has functions such as anti-apoptosis, anti-neurotoxicity, and antiinflammatory effects. Therapeutic approaches aimed at modulating or synergizing BDNF are anticipated to reduce inflammation and enhance outcomes in TBI patients. Magnesium sulfate administration is known for its anti-inflammatory and neuroprotective effects. Methods: This study employed a true experimental post-test-only group design. The subjects, male Wistar rats (Rattus norvegicus), were subjected to weight-drop-induced TBI and divided into three distinct groups: a control group (Group A), a TBI group without therapy (Group B), and a therapy group (Group C). Group B received TBI without magnesium sulfate administration, while Group C received TBI with magnesium sulfate administered at 250 μm/kg BW. BDNF levels in blood plasma were assessed at the conclusion of therapy utilizing ELISA. ANOVA was used to conclude the inquiry after all groups underwent a Shapiro-Wilk test. Results: Plasma BDNF levels were significantly lower in the TBI rat models treated with magnesium sulfate at 250 μm/kg BW within 4 hours after injury than in the untreated group (p = 0.005). Compared to the untreated group, the magnesium sulfate-treated group had reduced plasma BDNF levels. Conclusions: Administration of MgSO4 to the TBI treatment group resulted in decreased BDNF levels compared to the untreated group.