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Original Research Article | OPEN ACCESS

Abietic acid ameliorates neuroinflammation and blood-brain barrier disruption in traumatic brain injury by inhibiting MAPK pathway

Kongxue Xing1, Wenrong Jiang2

1Trauma Center, The Second People's Hospital of Ledong County, Ledong Li Autonomous County, Hainan Province 572536, China; 2Department of Neurosurgery, Haikou People's Hospital, Haikou, Hainan Province 570208, China.

For correspondence:-  Wenrong Jiang   Email: jwenrong0419@163.com   Tel:+8618189850718

Accepted: 27 August 2022        Published: 30 September 2022

Citation: Xing K, Jiang W. Abietic acid ameliorates neuroinflammation and blood-brain barrier disruption in traumatic brain injury by inhibiting MAPK pathway. Trop J Pharm Res 2022; 21(9):1893-1897 doi: 10.4314/tjpr.v21i9.12

© 2022 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

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.

Keywords: Abietic acid, MAPK pathway, Traumatic brain injury, Blood brain barrier, Neuroinflammation, Neurological deficit

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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