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

Traumatic brain injury (TBI) is a kind of physical damage that may result in either a permanent or temporary interruption of brain function, and it can be caused by a variety of events, including a bump, blow, or collision to the head. 1 Different geographic areas have varied rates of TBI.According to the Global Burden of Disease Study 2019, Africa has the lowest rate of traumatic brain injury, whereas North America and Europe have the greatest rate. 1 Because secondary brain injuries may vary in kind, including axonal injury, ischemic brain damage, and mass lesions, treatment options for them have not always been successful.Examples of these treatments include lipid peroxidation, apoptosis, glutamate excitotoxicity, free radical injury, edema, and calcium influx. 2 Hypoxia, hypotension, increased intracranial pressure, decreased blood perfusion to the brain 3 , and pyrexia are the main factors that cause secondary brain injury.Preventing secondary brain injury in cases of traumatic brain injury can enhance various outcomes. 4TBI may activate microglia and neuroinflammation, and cause damage to axons, neurons, and glia.Therefore, modifications to the intracellular proteins found in brain tissue or other organic compounds found in certain bodily fluids that serve as an indirect indicator of the ensuing brain injury and recovery are referred to as cerebral biomarkers. 1 The central nervous system (CNS) has systemic indicators that may be used to predict ABSTRACT 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 m/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 m/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.