Exploring the Therapeutic Potential of Tranexamic Acid for Traumatic Brain Injury: A Rat Model Study

Currently, there are no consistent findings regarding the effectiveness of Tranexamic Acid (TXA) treatment following traumatic brain injury (TBI) of varying severity. Anesthetized male Sprague-Dawley rats were divided into sham-operated, TBI (1.5 atm or 2.2 atm) + vehicle, and TBI + TXA groups. TXA was administered intraperitoneally at 0, 24, and 48 hours post-TBI at a dosage of 10 mg/kg/day for 3 consecutive days. Microglial and astrocyte activation, TNF-α expression, neuronal apoptosis, and cerebral injury volume on the ipsilateral side of the cortex were assessed using immunofluorescence or TTC staining. Brain edema and blood-brain barrier (BBB) permeability were evaluated using Evans blue injection, while motor function was assessed using the inclined plane test. The serum D-dimer was Pathological severity scores were evaluated using H.E. staining 72 hours after the initial injury. Compared with the TBI (1.5 atm and 2.2 atm) + vehicle group, the TBI + TXA 10 mg/kg group showed no significant improvement in motor dysfunction, reduction in body weight loss, decrease in BBB damage, or reduction in injury volume, neuronal apoptosis, or necrosis. Additionally, no significant decrease was observed in TBI-induced TNF-α expression in microglia and astrocytes, nor in pathological severity scores. Intraperitoneal administration of TXA at 10 mg/kg/day for three consecutive days did not show significant neuroprotective effects following TBI.