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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 ArticleDOI
TL;DR: It is suggested that central muscarinic receptor is a pharmacological target for the action of arecoline to modulate ethanol-induced hypnosis, and statistical analyses revealed that scopolamine (centrally acting) but not methscopolamines (peripherally acting), could antagonize the effect of are coline on the duration of ethanol- induced LORR.
Abstract: BACKGROUND: Epidemiological evidence of co-use of alcohol and areca nuts suggests a potential central interaction between arecoline, a major alkaloid of areca and a muscarinic receptor agonist, and ethanol. Moreover, the central cholinergic system plays an important role in the depressant action of ethanol and barbiturates. The purpose of this study was to investigate the effects of arecoline on pentobarbital- and ethanol-induced hypnosis in mice. METHODS: Male ICR mice were tested for locomotor activity following acute systemic administration of ethanol alone, arecoline alone, or ethanol plus arecoline. For the loss of the righting reflex (LORR) induced by pentobarbital and ethanol, sleep latency and sleeping duration were evaluated in mice treated with arecoline alone or the combination of arecoline and scopolamine or methscopolamine. RESULTS: Ethanol (1.0 to 3.0 g/kg, i.p.) reduced locomotor activity significantly and a declining trend was observed after treatment with arecoline (0.25 to 1.0 mg/kg, i.p.), but there were no synergistic effects of ethanol and arecoline on locomotor activity. The experiments on LORR demonstrated that arecoline (0.125 to 1.0 mg/kg, s.c.) shortened the duration of sleeping induced by ethanol (4.0 g/kg, i.p.), but not pentobarbital (45 mg/kg, i.p.). In addition, alterations of sleep latency were not obvious in both pentobarbital- and ethanol-induced LORR. Statistical analyses revealed that scopolamine (centrally acting), but not methscopolamine (peripherally acting), could antagonize the effect of arecoline on the duration of ethanol-induced LORR in mice. CONCLUSIONS: These results suggest that central muscarinic receptor is a pharmacological target for the action of arecoline to modulate ethanol-induced hypnosis.

7 citations

Journal ArticleDOI
Hong-Yan Ling1, Guang Wang1, Wei Zhang, Xing Li1, Shouhong Zhou1, Bi Hu1 
TL;DR: Arecoline treatment improves ACh-induced EDVR in high fructose-fed rats, and the potential mechanism of action might be associated with increase of CSE expression and activation of KATP channels by arecoline.
Abstract: Arecoline improves vascular endothelial function in high fructose-fed rats via increasing cystathionine-γ-lyase expression and activating K ATP channels

6 citations

Journal Article
TL;DR: The results indicate that the cholinergic mechanisms play an important role in thermoregulatory processes in rats and that the hypothermic effect of cholinomimetics is mediated through an activation of muscarinic Cholinergic receptors.
Abstract: The influence of various cholinergic drugs on rectal temperature of rats under controlled laboratory conditions was examined. Animals were anaesthetized by intraperitoneal injection of thiopental. Three hours later acetylcholine, methacholine, arecoline, nicotine, neostigmine, atropine, methylatropine, mecamylamine or hemicholinium were injected intrahypothalamically (i.h.), intracerebroventricularly (i.c.v.) or intraperitoneally (i.p.). Rectal temperature was measured at 15 min-intervals for 1 hr after the substances were injected. Our results indicate that the cholinergic mechanisms play an important role in thermoregulatory processes in rats. Cholinergic activation decreases rectal temperature, due to an increased activity of central, and not of peripheral cholinergic neurotransmission. The hypothermic effect of cholinomimetics is mediated through an activation of muscarinic cholinergic receptors.

6 citations

Journal ArticleDOI
TL;DR: In this paper, an extensive quantification of the components with varying concentrations of areca nut extract and commercial smokeless tobacco products have been done, and the results showed increased collagen production.
Abstract: Introduction: Extracellular matrix component derangement is the major event in pathogenesis of Oral submucous fibrosis. Many studies have elaborated the alteration of the matrix components at a cellular and genetic level. However elaborate quantification of the components with varying concentrations of Areca nut extract and commercial tobacco products have not been done so far. Materials and Methods: Primary culture of tissues sourced during crown lengthening procedures were used for establishment of fibroblast monoculture and fibroblast / keratinocyte co-culture. Extracts of areca nut, commercial smokeless tobacco products (gutkha and haans) and control CCl4 were tested at concentrations ranging from 20 μL, 40 μL, 80 μL, 160 μL, 320 μL and time intervals of 12, 24, 48, 72 hours. Collagen quantification by spectrophotometry and SNAI1 gene expression study were done. Results: Extract of areca nut was found to show increased collagen production than commercial tobacco products and closely similar values to CCL4. Kruskal Wallis test was used to analyse the difference in collagen obtained. The mean values of collagen obtained in co-culture were lesser than those obtained in the fibroblast monoculture. SNAI1 gene expression was negative in both the culture experiments. Conclusion: Areca nut extract was found to be more potent as an individual agent. Commercial smokeless tobacco products Gutka and Hans exhibited increased collagen production at higher concentration. These findings further steps up the persuasive ill effects of tobacco products. Negative SNAI1 gene expression was corroborated to lack of extracellular environment in the co coculture experiment.

6 citations

Journal Article
TL;DR: A review of literature on the health effects of arecanut chewing shows that it is not carcinogenic in normal dose as mentioned in this paper. But, it is sad to note that such reports were sidelined by most of the researchers and reviewers.
Abstract: Review of literature on the health effects of arecanut chewing shows that it is not carcinogenic in normal dose. It was reported that an adult human being masticate up to 0.5g of arecanut/kg bw/day. Animal studies have revealed that feeding of processed arecanut (dried or boiled) at 1.0g/kg body weight/day and pan masala up to 1.67g/kg bw/day were safe for mice. Arecanut paste when applied to bare skin at 1.5g /kg bw/day was safe for hamsters. Feeding of arecoline, the physiologically most active chemical compound of arecanut, was found safe for mice at 100mg/kg bw/day. The LD50 value for arecanut extract was reported to be >15,000mg/kg bw for rats. The betel quid at a concentration of 0.1ml of 2% solution without tobacco was also found safe for mice. The arecanut and betel quid extracts without tobacco were even reported to retard the development of tumors in mice and cure breast cancer cells, gastric cancer cells and liver cancer cells in human being. Several population studies carried out in India and abroad on the effects of chewing betel quid without tobacco did not show any significant harmful effects on human health. It is really sad to note that such reports were sidelined by most of the researchers and reviewers.

6 citations


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