Boswellic Acid Attenuates Scopolamine-Induced Neurotoxicity and Dementia in Rats: Possible Mechanism of Action

Background and Objective: The oleo gum resin of plants belonging to the Boswellia species contains pentacyclic triterpenic acids known as boswellic acid. This acid possesses anti-depressive, anti-anxiety, anti-tumour, neuroprotective, antioxidant and anti-inflammatory activities. This research work was undertaken to assess the neuroprotective effects of boswellic acid in scopolamine-treated rats. Materials and Methods: Wistar rats were grouped equally into four groups. Groups I and II received 0.5 mL saline, while animals from Group III and IV received boswellic acid (40 and 80 mg kg–1/day, respectively) for 21 days, intraperitoneally (i.p.). One hour after the respective treatments, daily 0.5 mL of normal saline was given intra-peritoneally to normal control animals and scopolamine (2 mg kg–1/day, i.p.) was given to all other animals. Results: On day 21, after 30 min of scopolamine treatment, animals were evaluated for behavioural parameters. Then animals were euthanized and brains were used for biochemical studies and RNA expression analysis. Conclusion: Treatment with scopolamine altered the normal behaviours, impaired memory and decreased the mRNA expressions of Brain-Derived Neurotrophic Factor (BDNF), Ca2+/calmodulin-dependent protein kinase(CaMK), Cyclic adenosine monophosphate (cAMP), cAMP-response element-binding (CREB), Extracellular Signal-regulated Kinase (ERK) and Phosphoinositide 3-kinases (PI3K) as well as increased oxidative stress and AchE activity in brain tissue. Whereas, pretreatment with boswellic acid to scopolamine treated animals corrected the altered behaviour, decreased oxidative stress and Acetylcholinesterase (AchE) activity, restored memory, antioxidant capacity and BDNF, CaMK, CREB, ERK and PI3K mRNA expression. These results indicate the protective actions of boswellic acid in scopolamine-induced dementia in rats. Significant free radical scavenging potential points out toward neuroprotective action.