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Arecoline

About: Arecoline is a research topic. Over the lifetime, 744 publications have been published within this topic receiving 16015 citations. The topic is also known as: methylarecaiden & methylarecaidin.


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Journal Article
TL;DR: Arecoline is able to induce Hacat cell apoptosis, which may contribute to the development of oral submucous fibrosis.
Abstract: Objective To observe the effect of arecoline on the apoptosis of Hacat cellsMethods Hacat cells were incubated with different concentrations of arecoline(0,25,50,75,100 or 125 μg/mL) for 24 hDNA fragments and apoptosis were examined by agarose gel electrophoresis and flow cytometry,respectivelyResults DNA fragments were obviously observed in groups treated with arecoline in a concentration of 100 or 125 μg/mLThe results of flow cytometry showed that arecoline induced apoptosis in a dosedependent mannerConclusion Arecoline is able to induce Hacat cell apoptosis,which may contribute to the development of oral submucous fibrosis

2 citations

Journal ArticleDOI
TL;DR: Molecules with electron donating group as a substitute, has shown very good affinity towards the M1 receptor in vitro and has also elicited beneficial effects in vivo memory and learning models.
Abstract: T cholinergic deficit in Alzheimer’s disease (AD) patient’s brain has intensified research efforts to test cholinomimetic approaches for efficacy in AD therapy. Various therapies may be of potential clinical use in AD. Among these are cholinergic agents including muscarinic agonists, acetylcholinesterase inhibitors, and acetylcholine releasing agents. One of the muscarinic agonists tested in AD is arecoline and its bioisosters, which are widely, explored as muscarinic receptor 1 agonist (M1 receptor agonist) in AD research. In this regard, we have synthesized five and six membered heterocyclic ring system attached arecoline basic nucleus (N-methyl tetrahydropyridines) at 3rd position. Subsequently the synthesized arecolines derivatives were subjected to in vitro muscarinic receptor 1 binding affinity studies using male wistar rat brain synaptosomal membrane (cerebral cortex) and also cell line culture studies and extended this in vitro studies to in vivo pharmacological evaluation of memory and learning in male wistar rats (Rodent memory evaluation, plus and Y maze studies). Some of our synthesized molecules have shown very potent M1 receptor agonist activity and significantly elevated the basal IP3 levels in vitro and also have decreased beta-amyloid (Abeta40 and Abeta42) deposition in cell lines culture. These molecules have also shown very good antidementia activity in rat dementia model. Conclusions: Molecules with electron donating group as a substitute, has shown very good affinity towards the M1 receptor in vitro and has also elicited beneficial effects in vivo memory and learning models. Muscarinic Receptor 1 Agonist Activity of Novel Arecoline Derivatives in Alzheimer’s Dementia Models

2 citations

Journal ArticleDOI
01 Nov 2022
TL;DR: In this paper , the effects of four primary alkaloids (arecoline, arecaidine, guvacine, and guvacanoline) isolated from areca nut on zebrafish larvae were investigated.
Abstract: Areca palm nut (Areca catechu) has been listed as one of the most addictive substances, along with tobacco, alcohol, and caffeine. It belongs to the family Arecaceae and is widely used in Asia. Areca nut contains seven psychoactive alkaloids; however, the effects of these alkaloids on behaviors are rarely to be addressed in zebrafish. Therefore, this study aims to compare the psychoactive and potential adverse effects of four primary alkaloids (arecoline, arecaidine, guvacine, and guvacoline) isolated from areca nut on zebrafish. We found that four alkaloids induced hyperactivity-like behaviors in zebrafish larvae. Cooperating the results with the previous study, molecular docking scores suggested these alkaloids might bind to multiple muscarinic acetylcholine receptors (mAChRs), and various best binding modes were shown. According to the adult zebrafish behavioral test, arecoline was found to slightly increase the locomotor activity and caused tightening shoaling formations of adult zebrafish. Meanwhile, zebrafish exposed to arecaidine have reduced aggressiveness and conspecific social interaction. Similar to arecaidine, guvacoline treatment also caused abnormalities in zebrafish social behaviors. Furthermore, the fish displayed abnormal exploratory behaviors after being exposed to guvacoline. Interestingly, altered fear response behaviors were only displayed by guvacine-treated fish besides their lower locomotor activity. Based on the results of molecular docking, we hypothesize that the behavior alterations might be a consequence of the interaction between alkaloids and multiple mAChRs in the nervous system. In summary, our study found that each alkaloid specifically affects adult zebrafish behaviors.

2 citations

Journal Article
TL;DR: The results suggest that pilocarpine and arecoline act as ACh-releaser in this tissue and that the ouabain-induced cholinergic potentiation may be attributable to a dual mechanism, facilitation of ACh release at presynaptic site and alteration of the membrane excitability at postsynaptic site.
Abstract: In the guinea-pig vas deferens, the contractions induced by pilocarpine and arecoline, unlike ACh, were markedly reduced by treatment with procaine (10(-6) g/ml) or hemicholinium (5 x 10(-4) g/ml). These reductions by hemicholinium were completely recovered after exposure to choline. The contractile responses to these three agonists were eliminated by atropine (3 x 10(-8) g/ml) but enhanced by neostigmine (3 x 10(-8) g/ml), though these were not affected at all by tetrodotoxin (3 x 10(-8) g/ml) or hexamethonium (10(-5) g/ml). The contractile responses to ACh, pilocarpine and arecoline were potentiated by ouabain (10(-6) g/ml). These potentiations were more marked in pilocarpine and arecoline than those in ACh. The potentiation in response to arecoline was maximal after incubation with ouabain for 5 min but that to ACh for 45 min. The results suggest that pilocarpine and arecoline act as ACh-releaser in this tissue and that the ouabain-induced cholinergic potentiation may be attributable to a dual mechanism, facilitation of ACh release at presynaptic site and alteration of the membrane excitability at postsynaptic site.

2 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202335
202243
202126
202038
201921
201818