Abstract
Purpose: To investigate the effects of abietic acid (AA) on traumatic brain injury (TBI) in a rat model, and the underlying mechanisms of action.
 Methods: Twenty male Sprague-Dawley (SD) rats were randomly divided into four groups of 5 animals each: Sham, TBI, TBI + AA (14 mg/kg), and TBI + AA (28 mg/kg). Controlled cortical impact (CCI) model was used to induce TBI in rats. Western blot was used to determine the protein levels of Claudin 3, Occludin, ZO-1, Bax, Bcl-2, cleaved-caspase3, p65 NF-κB, p-p65 NF-κB, ERK, p-ERK, JNK, p-JNK, p38 and p-p38, while the expressions of TNF-α, IL-6 and IL-1β were determined using the applicable assay kits. Neurological deficit was assessed based on mNSS and brain water content.
 Results: Treatment with AA significantly reduced TBI-induced blood-brain barrier (BBB) damage, as well as apoptosis and neuroinflammation in a concentration-dependent manner (p < 0.001). The neuroprotective effect of AA was associated with the inhibition of the MAPK signaling pathways and subsequent suppression of NF-κB (p < 0.001).
 Conclusion: Abietic acid serves as a potential novel candidate for the treatment of TBI, and its anti-inflammatory and anti-apoptotic effects are related to the suppression of MAPK signaling pathways. Therefore, abietic acid may serve as a novel candidate for the treatment of TBI in humans.
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