Topic
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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TL;DR: A case-control study of oral squamous cell carcinoma patients and controls was conducted to evaluate the gene-environment interaction between COX-2 promoter polymorphisms and substance use of alcohol, betel quid, and cigarettes (ABC) in risk of OSCC, including ANE/sANE-induced transcriptional effects and enhanced joint effects of COx-2 -1195A allele with substanceUse of ABC.
Abstract: Because the mRNA expression of cyclooxygenase-2 (COX-2) is up-regulated by arecoline in human gingival fibroblasts, as shown in our previous study, we further investigated the mRNA expression level of COX-2 and its upstream effectors in three oral epithelial carcinoma cell lines (KB, SAS, and Ca9-22) by using areca nut extract (ANE) and saliva-reacted ANE (sANE). A case-control study of 377 oral squamous cell carcinoma (OSCC) patients and 442 controls was conducted to evaluate the gene-environment interaction between COX-2 promoter polymorphisms and substance use of alcohol, betel quid, and cigarettes (ABC) in risk of OSCC. The heterogeneous characteristics of the oral site and the COX-2 -1195G>A polymorphism in these cell lines showed diverse inflammatory response (KB>>Ca9-22>SAS) after 24-hour ANE/sANE treatments, and the COX-2 up-regulation might be mostly elicited from alternative nuclear factor-kappaB activation. In the case-control study, betel chewing [adjusted odds ratios (aOR), 42.2] posed a much higher risk of OSCC than alcohol drinking and cigarette smoking (aORs, 2.4 and 1.8, respectively), whereas the COX-2 -1195A/A homozygote presented a potential genetic risk (OR, 1.55). The strongest joint effect for OSCC was seen in betel chewers with -1195A/A homozygote (aOR, 79.44). In the non-betel chewing group, the -1195A/G and A/A genotypes together with the combined use of alcohol and cigarettes increased risk to 15.1-fold and 32.1-fold, respectively, compared with the G/G genotype without substance use. Taken together, these findings illustrate a valuable insight into the potential role of the COX-2 promoter region in contributing to the development of betel-related OSCC, including ANE/sANE-induced transcriptional effects and enhanced joint effects of COX-2 -1195A allele with substance use of ABC.
68 citations
TL;DR: It is concluded that increased mRNA expression of TIMP-1 in buccal mucosal fibroblasts by arecoline and safrole is a possible pathogenesis for oral submucous fibrosis.
68 citations
TL;DR: A tentative model to explain arecoline-induced effects on contribution of oral pathogenesis is proposed and the findings identified that 12 susceptible genes can potentially serve as biomarkers of arecolin-induced damage in betel chewers.
67 citations
TL;DR: Mood, behavioral, and neurochemical responses to arecoline, which appears to have nonspecific neurochemical effects at the dose employed, are not markers of vulnerability to affective illness.
Abstract: Cholinergic supersensitivity has been postulated to be an etiologic factor in affective disorder. After several pilot dose-response studies, we administered 8 mg of the cholinergic agonist arecoline subcutaneously to eight pairs of normal volunteer identical twins and eight bipolar patients currently euthymic and unmedicated. During the hour following arecoline administration, the Profile of Mood States (POMS) showed an increase in total mood disturbance in both patient and control groups. Mean systolic blood pressure, pulse, plasma cortisol, prolactin, and growth hormone also increased. Anger and elation scores on the POMS showed significant concordance in identical twins, as did change in prolactin, implying that these are the components of drug response possibly influenced by genetic factors. None of these responses differentiated well state patients from controls. Thus, mood, behavioral, and neurochemical responses to arecoline, which appears to have nonspecific neurochemical effects at the dose employed, are not markers of vulnerability to affective illness.
67 citations
TL;DR: A muscarinic cholinergic mediation of passive avoidance learning through the synaptic elements located in the basal lateral part of the amygdala in the young rat is suggested.
Abstract: Passive avoidance learning was studied in young rats 13–30 days of age following bilateral injections of saline or antimuscarinic and/or muscarinic agents into three amygdaloid nuclei — lateral (L), basolateral (BL), and cortical (CO). While acquisition was not influenced by saline injections into various other cerebral structures, it was significantly altered by similar injections into these amygdaloid nuclei, especially by those into the BL nucleus, suggesting that this nucleus is particularly involved in passive avoidance learning. Atropine induced significant deficits from as early as 13 days on. These deficits increased and were of similar strength after injections into any of the three studied nuclei until day 16; after that age, they diminished slightly following CO and L nuclei administration, while remaining substantial after BL nucleus injections at all ages, even at 30 days. No facilitatory effects could be elicited by arecoline injected alone, while arecoline could antagonize the disturbing effect of atropine, when given in combination, from day 13 on. These results suggest a muscarinic cholinergic mediation of passive avoidance learning through the synaptic elements located in the basal lateral part of the amygdala in the young rat.
66 citations