3-O-Acetyl-11-keto-β-boswellic acid ameliorates acquired, consolidated and recognitive memory deficits through the regulation of hippocampal PPAR γ, MMP9 and MMP2 genes in dementia model

Abstract

Pentacyclic Phytomolecule 3-O-Acetyl-11-keto-β-boswellic acid (AKBA) from Frankincense family has proven for the neuroprotection and recognized as an orphan drug for the treatment of cerebral edema. Nonetheless, AKBA have promising indications with Peroxisome proliferator activated receptor gamma (PPARγ) associated to cognitive function not deliberated so far. In order to substantiate the potential role of AKBA on memory function, we examine the contribution of PPARγ activation and its downstream process. Modified method of scopolamine induced dementia rats were treated with AKBA (5, 10&15 mg/kg,i.p) and Donepezil (2.5 mg/kg,i.p). Scopolamine induced short term spatial, working memory and recognition memory impairment was reversed significantly after AKBA treatment. AKBA administration diminished the Acetylcholine esterase (AchE) activity and preserved brain GABA and glutamate mediated neuronal excitability. Further, gene expression study reveals AKBA ameliorates the memory impairment via activating PPARγ and its downstream regulators, matrix metalloproteinase 2 (MMP2) and matrix metalloproteinase 9 (MMP9) genes in hippocampus. This study concludes that the treatment with AKBA can be a novel Phyto-molecule of interest for treating dementia via up-regulating hippocampus genes mediated cholinergic activation.

Glycyrrhizin and boswellic acids, the golden nutraceuticals: multitargeting for treatment of mild–moderate COVID-19 and prevention of post-COVID cognitive impairment

“…Another study indicated that a possible mechanism for the beneficial effects of BAs may include inhibition of the 5-LOX/COX pathway in arachidonic acid metabolism, activation of Nrf2 (has anti-inflammatory activity), through binding to ARE (antioxidant response element) and inhibition of NF-kB (Siddiqui et al 2021 ). Furthermore, BAs eliminate memory impairment by enhancing the activity of PPARγ and its downstream regulators, matrix metalloproteinase 2 genes in the hippocampus (Gunasekaran et al 2021 ). In a double-blind, randomized, placebo-controlled clinical trial, the effect of BAs on cognitive impairment after traumatic brain injury (TBI) was investigated.…”

Minocycline alleviated scopolamine-induced amnesia by regulating antioxidant and cholinergic function

“…An amnesic rat model was created by the administration of scopolamine (2 mg/kg in saline; IP). Duration and dose of scopolamine injection were determined according to recent investigations [ 19 , 22 , 21 ]. The treatment groups (groups 3–6) received 10, 15, 20, or 30 mg/kg of minocycline, whereas the scopolamine group and group 1 received the vehicle for two weeks [ 23 , 10 ].…”

“…Evidence suggests multiple neuroprotective mechanisms of minocycline in different pathological conditions [ 12 ]. Noticeably, scopolamine attenuates the activity of the cholinergic system in the brain tissue [ 19 , 20 ]. Hence, in the present study, we investigated whether treatment with minocycline can reverse scopolamine-mediated memory deficits via AChE and oxidative stress markers in the brain.…”