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Showing papers on "Arecoline published in 2005"


Journal ArticleDOI
TL;DR: It is demonstrated that IGF-1 expression is significantly upregulated in OSF from areca quid chewers and arecoline may be responsible for the enhanced IGF- 1 expression in vivo.

49 citations


Journal ArticleDOI
TL;DR: The hypothesis that chronic exposure of the fetus to arecoline (the principal alkaloid of the areca nut) is the cause was investigated in a clinical observational study on six newborns from Asian mothers who chewed betel nut during pregnancy.
Abstract: The betel nut is commonly used as a drug by Asian populations. A high prevalence of adverse pregnancy outcomes has been reported in women who chewed betel quid during gestation. The hypothesis that chronic exposure of the fetus to arecoline (the principal alkaloid of the areca nut) is the cause was investigated in a clinical observational study on six newborns from Asian mothers who chewed betel nut during pregnancy.

47 citations


Journal ArticleDOI
TL;DR: The results indicate that arecoline would decrease vascular tone, in part mediated by NO, which suggest that long-term use or high doses of areca nut might induce endothelial dysfunction and associated diseases.
Abstract: This study investigated the effects of arecoline, an active ingredient of the areca nut, on the tone of human umbilical arteries and veins and on the eNOS expression and cell proliferation of human umbilical vein endothelial cells (HUVECs). We found that arecoline relaxes the human umbilical artery and vein rings in a concentration-dependent manner; the higher the concentration of arecoline, the greater the relaxation of the rings. However, the relaxation decreases after the endothelium was removed or pretreated with L-NAME, a nitric oxide synthase inhibitor. Moreover, arecoline increases in a dose-dependent way the cGMP levels of human umbilical arteries and veins. In HUVECs, arecoline also increases the eNOS expression. Therefore, the relaxant effects of arecoline on the umbilical artery and vein rings were endothelium-dependent through the NO-cGMP systems. In addition, arecoline at higher doses (100-1000 microM) inhibits endothelial cell proliferation; the exposure toarecoline (100-1000 microM) for 24 and 48 h induces G2/M cell cycle arrest of HUVECs. Our results indicate that arecoline would decrease vascular tone, in part mediated by NO. Higher doses of arecoline inhibit endothelial cell growth, which suggest that long-term use or high doses of areca nut might induce endothelial dysfunction and associated diseases.

29 citations


Journal ArticleDOI
TL;DR: It is suggested that KGF-1 expression is significantly upregulated in OSF tissues from areca quid chewers and arecoline may be responsible for the enhanced KGF -1 expression in vivo.
Abstract: Background: Keratinocyte growth factor-1 (KGF-1) is the seventh member of the fibroblast growth factor family. KGF-1 is produced by mesenchymal cells such as fibroblasts and upregulated in a variety of hyperplastic tissues. Currently, there is limited information about the regulation of KGF-1 expression in areca quid-associated oral submucous fibrosis (OSF). The aim of the study was to compare KGF-1 expression in normal human buccal mucosa and OSF specimens and further to explore the potential mechanism that may lead to induce KGF-1 expression. Methods: The expression of KGF-1 from fibroblasts cultured from OSF and normal buccal mucosa were using reverse-transcriptase polymerase chain reaction and enzyme-linked immunosorbent assay. In addition, arecoline, a major areca nut alkaloid, was challenged to normal buccal mucosa fibroblasts (BMFs) to elucidate whether KGF-1 expression could affect by arecoline. Furthermore, 25 OSF specimens and six normal buccal mucosa specimens were examined by immunohistochemistry. Results: Fibroblasts derived from OSF were found to exhibit higher KGF-1 expression than BMFs both in mRNA and protein levels (P < 0.05). In addition, upregulation of KGF-1 mRNA gene and protein expression were found in BMFs stimulated by arecoline (P < 0.05). From the results of immunohistochemistry, KGF-1 expression was significantly higher in OSF specimens and expressed mainly by fibroblasts, endothelial cells, inflammatory cells, and epithelial cells. Conclusions: Taken together, these results suggest that KGF-1 expression is significantly upregulated in OSF tissues from areca quid chewers and arecoline may be responsible for the enhanced KGF-1 expression in vivo.

29 citations


Journal ArticleDOI
TL;DR: The inhibition of areca nut on phagocytosis of neutrophils may be one possible mechanism by which the areca nuts compromises the periodontal health of areCA quid chewers.
Abstract: Background: Areca quid chewers have a higher prevalence of periodontal disease than non-chewers. Little is known about the influence of areca quid on the immune system. This study was to determine the possible effects of the areca nut on phagocytic activity of human neutrophils. Methods: Aqueous extracts of ripe areca nut without husk (rANE), fresh and tender areca nut with husk (tANE), a major alkaloid (arecoline), and a phenolic component ([+]-catechin) of areca nut were examined for their effects on cellular viability using trypan blue exclusion assay. The possible effects on the phagocytic activity of neutrophils against a periodontal pathogen, Actinobacillus actinomycetemcomitans ATCC 33384, were determined using flow cytometry and confocal laser scanning microscopy. Results: At the concentrations tested, rANE, tANE, arecoline, and (+)-catechin did not significantly affect viability of neutrophils. However, rANE, tANE, arecoline, and (+)-catechin inhibited the phagocytic activity of neutrophils in a ...

23 citations



Journal ArticleDOI
TL;DR: The results suggest that AQ consumption may promote oral tumor progression through the induction of MMP-2 secretion in most oral tumor patients with long-term AQ usage.

19 citations


Patent
03 Jun 2005
TL;DR: In this paper, a composition comprising a nicotinic receptor agonist and method for preventing and treating inflammatory diseases related to body inflammation including arthritis, cutaneous inflammation and cardio-vascular inflammatory related diseases is presented.
Abstract: The present invention relates to a composition comprising a nicotinic receptor agonist and method for preventing and treating inflammatory diseases related to body inflammation including arthritis, cutaneous inflammation and cardio-vascular inflammatory related diseases. Particular nicotinic receptor agonist disclosed for the treatment and prevention of arthritis, cutaneous inflamation and cardiovascular inflamatory related diseases include dimethylphenylpiperazinium (DMPP), nicotine, epibatidine, cytisine, mecamylamine, acetylcholine, pyridlethers, tubocurarine, trimethaphan, hexamethonium, N-methylcaramylcholine, ABT-418, GTS-21, MLA, DHβE, Arecoline, lobeline, philanthotoxin-433, azabicyclin, SIB-1553, and imidacloprit.

6 citations


Journal Article
TL;DR: Salvia Miltiorrhizae could downregulate the arecoline-induced apoptosis of VEC and maintain integrity of endothelium, suggesting that SM may posses antifibrotic ability.
Abstract: [Objective]To investigate the effects of Salvia Miltiorrhizae (SM) on the apoptosis of vascular endothelia cells(VEC) induced by arecoline and the activity of Caspase-3. Human Umbilical Vein Endothelial Cells(HUVECs) were cultured in vitro. Apoptosis of VEC were induced by arecoline, and SM was added in test specimen. Apoptotic morphological changes and percentage of apoptosis were observed under fluorescent microscope. The activity of Caspase-3 were evaluated by the colorimeteric assay. Compared with control, VEC apoptosis increased significantly and the activity of Caspases-3 increased in arecoline(90ug/ml) group. SM(8mg/ml) reduced the apoptosis induced by arecoline (P 0.05) and the activity of Caspases-3. [Conclusion] SM could downregulate the arecoline-induced apoptosis of VEC and maintain integrity of endothelium, suggesting that SM may posses antifibrotic ability.

1 citations


Journal Article
TL;DR: Arecoline may induce the apoptosis of HUVECs and caspase-3 takes part in the control of apoptotic process.
Abstract: Objective: The purpose of the study is to investigate the mechanism of the change of caspase-3 activity on the arecoline-induced apoptosis in endothelial cells(EC). Methods: HUVECs were cultured in virto. Apoptosis of HUVECs were induced by arecoline. The changes of apoptotic cells and caspase-3 activity in EC were evaluated with the fluorescecet microscopy and the colorimeteric assay respectively and were compared with normal control group. Results: Obvious cell apoptotic change could be observed with fluorecent microscopy after arecoline stimulation; The level of caspase-3 activity was significantly higher in the arecoline group than that of normal control group(P0.01). Conclusion: Arecoline may induce the apoptosis of HUVECs and caspase-3 takes part in the control of apoptotic process.

1 citations