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Trauma/Critical Care Rapid Fire Abstract Session

Trauma

3-Acetyl-11-Keto-β-Boswellic Acid (AKBA) Attenuates Neuroinflammation in a Mouse Model of Traumatic Brain Injury

Saturday, May 4, 2024
1:41 PM – 1:43 PM CT
Location:  S405a
Disclosure(s):
Lea Scherschinski, MD: No financial relationships to disclose
Michael T. Lawton, MD: No financial relationships to disclose
Introduction: Traumatic Brain Injury (TBI) results from external head trauma, causing various symptoms based on injury severity. TBI is a significant public health concern, with approximately 166 individuals succumbing to TBI daily. Inflammation is a pivotal factor in TBI, and AKBA (acetyl-11-keto-β-boswellic acid), a bioactive pentacyclic triterpene, is known for its potential in mitigating ischemic insults and providing neuroprotection in neurodegenerative diseases. With its antioxidant and anti-inflammatory properties, this study investigates AKBA as a novel therapeutic approach for TBI management.

Methods: A closed head injury (CHI) model was used to induce repetitive mild traumatic brain injury (rmTBI) in C57BL/6 mice. Subsequently, mice were treated with AKBA for 5 consecutive days, and blood plasma and brain tissue samples were harvested from 3 distinct groups: Sham, TBI, and TBI+AKBA. Cerebral blood flow (CBF) was quantified using laser speckle imaging. Various plasma biomarkers, including C3a and Neutrophil Extracellular Traps (NETs) markers (MPO, ELA2, and CitH3), TNF-α, IL-6, and IL-10, were assessed using ELISA and flow cytometry. The levels of C3a receptor, Iba-1 (a microglial marker), GFAP, and cell death were examined through western blotting, immunohistochemistry, and TUNEL assay. Cognitive function was evaluated using the novel object recognition test (NORT).

Results: AKBA treatment significantly improved the CBF compared to the TBI group. Furthermore, AKBA treatment resulted in significant reductions in the expression levels of Iba-1, GFAP, and NETs markers in both brain and blood samples. TUNEL assay results indicated a significant decrease in cell death within the AKBA-treated TBI group compared to the TBI group alone. Additionally, flow cytometry data showed decreased neutrophil infiltration. Our NORT data demonstrated that AKBA treatment improved cognitive function in TBI mice.

Conclusion : Our data suggests that AKBA treatment has the potential to mitigate neuroinflammation in TBI and could serve as a promising candidate for the development of new therapeutics for TBI management.