Title:Neuro-protective Effect of Acetyl-11-keto-β-boswellic Acid in a Rat Model of
Scopolamine-induced Cholinergic Dysfunction
Volume: 30
Issue: 2
Author(s): Amir Hossein Assaran, Mahmoud Hosseini, Matin Shirazinia, Mohammad Hosein Eshaghi Ghalibaf, Farimah Beheshti, Leila Mobasheri, Farshad Mirzavi and Arezoo Rajabian*
Affiliation:
- Neuroscience Research Center, Mashhad University of Medical Sciences,
Mashhad, Iran
- Department of Neuroscience, Faculty of Medicine, Mashhad
University of Medical Sciences, Mashhad, Iran
Keywords:
Bcl-2, cholinergic function, oxidative stress, brain-derived neurotrophic factor, apoptosis, acetyl-11-keto-β-boswellic acid.
Abstract:
Background: Acetyl-11-keto-β-boswellic acid (AKBA) is a major component of the oleo-gum
resin of B. serrata with multiple pharmacological activities. The objective of this study was to explore the underlying
mechanisms of neuroprotective potential of AKBA against scopolamine-mediated cholinergic dysfunction
and memory deficits in rats.
Methods: The rats received AKBA (2.5, 5, and 10 mg/kg, oral) for 21 days. In the third week, scopolamine
was administered 30 min before the Morris water maze and passive avoidance tests. In order to perform biochemical
assessments, the hippocampus and prefrontal cortex were extracted from the rats euthanized under
deep anesthesia.
Results: In the MWM test, treatment with AKBA (5 and 10 mg/kg) decreased the latency and distance to find
the platform. Moreover, in the PA test, AKBA remarkably increased latency to darkness and stayed time in
lightness while decreasing the frequency of entry and time in the darkness. According to the biochemical assessments,
AKBA decreased acetylcholinesterase activity and malondialdehyde levels while increasing antioxidant
enzymes and total thiol content. Furthermore, AKBA administration restored the hippocampal mRNA
and protein levels of brain-derived neurotrophic factor (BDNF) and mRNA expression of B-cell lymphoma (Bcl)-
2 and Bcl-2- associated X genes in brain tissue of scopolamine-injured rats.
Conclusion: The results suggested the effectiveness of AKBA in preventing learning and memory dysfunction
induced by scopolamine. Accordingly, these protective effects might be produced by modulating BDNF, cholinergic
system function, oxidative stress, and apoptotic markers.
