Evaluation of the Neuroprotective Role of Boric Acid in Preventing Traumatic Brain Injury-Mediated Oxidative Stress

AIM: To investigate the possible neuroprotective effect of boric acid (BA) by examining the changes in catalase (CAT) activity and levels of CAT and malondialdehyde (MDA) in brain tissues from rats with closed head trauma. MATERIAL and METHODS: The study consisted of three groups: control, traumatic brain injury (TBI) and TBI + BA. Animals in the control and TBI groups received saline, while animals in the TBI + BA group received BA through daily oral gavage, for 14 days prior to TBI was performed using the modified Marmarou impact acceleration model. After 24 hours, animals were euthanized, and brain tissue obtained to measure the levels of MDA and to assess the activity of CAT. RESULTS: MDA levels and CAT activity were significantly higher in the TBI group versus the control group. However, they were significantly lower in the TBI + BA group compared to TBI alone. Similarly, edema and necrotic neurons were observed in the TBI group, but not in the control or TBI + BA groups. CONCLUSION: Based on biochemical and histopathological evidence, we determined that TBI induced lipid peroxidation and oxidative stress were inhibited by pre-treatment with BA.

Automated summary

Boric acid may have a neuroprotective effect by reducing lipid peroxidation and increasing catalase activity in brain tissues of rats with closed head trauma. Results show that pre-treatment with boric acid can decrease malondialdehyde levels and improve tissue structure, thus inhibiting the oxidative stress response induced by traumatic brain injury.