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Pesquisa : D03.066.515.292 [Categoria DeCS]
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[PMID]:29385191
[Au] Autor:Chuerduangphui J; Ekalaksananan T; Chaiyarit P; Patarapadungkit N; Chotiyano A; Kongyingyoes B; Promthet S; Pientong C
[Ad] Endereço:Department of Microbiology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
[Ti] Título:Effects of arecoline on proliferation of oral squamous cell carcinoma cells by dysregulating c-Myc and miR-22, directly targeting oncostatin M.
[So] Source:PLoS One;13(1):e0192009, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Arecoline, the major alkaloid of areca nut, is known to induce oral carcinogenesis, however, its mechanism is still needed to elucidate. This study investigated the effects of arecoline on cell viability and cell-cycle progression of oral squamous cell carcinoma (OSCC) cells as well as a relevant cellular gene expression. The results showed that a low concentration of arecoline (0.025 µg/ml) increased OSCC cell viability, proportion of cells in G2/M phase and cell proliferation. Simultaneously, it induced IL-6, STAT3 and c-Myc expression. Interestingly, c-myc promoter activity was also induced by arecoline. MiR-22 expression in arecoline-treated OSCC cells was suppressed and comparable to an upregulated c-Myc expression. In arecoline-treated OSCC cells, oncostatin M (OSM) expression was significantly upregulated and inversely correlated with miR-22 expression. Likewise, OSM expression and its post-transcriptional activity were significantly decreased in miR-22-transfected OSCC and 293FT cells. This result demonstrated that miR-22 directly targeted OSM. Interestingly, miR-22 played an important role as a tumor suppresser on suppressing cell proliferation, migration and cell-cycle progression of OSCC cells. This result suggested the effect of arecoline to promote cell proliferation and cell-cycle progression of OSCC cells might be involved in induction of c-Myc expression and reduction of miR-22 resulting in OSM upregulation.
[Mh] Termos MeSH primário: Arecolina/farmacologia
Carcinoma de Células Escamosas/patologia
Proliferação Celular/efeitos dos fármacos
MicroRNAs/metabolismo
Neoplasias Bucais/patologia
Proteínas Proto-Oncogênicas c-myc/metabolismo
[Mh] Termos MeSH secundário: Carcinoma de Células Escamosas/metabolismo
Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Seres Humanos
Interleucina-6/biossíntese
MicroRNAs/genética
Neoplasias Bucais/metabolismo
Regiões Promotoras Genéticas
Proteínas Proto-Oncogênicas c-myc/genética
Fator de Transcrição STAT3/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-6); 0 (MIRN22 microRNA, human); 0 (MicroRNAs); 0 (Proto-Oncogene Proteins c-myc); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 4ALN5933BH (Arecoline)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0192009


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[PMID]:28245263
[Au] Autor:Chen CH; Lu HI; Wang YM; Chen YH; Lo CM; Huang WT; Li SH
[Ad] Endereço:Institute for Translational Research in Biomedicine, Kaohsiung Chang Gung Memorial Hospital and Department of Applied Chemistry, and Graduate Institute of Biomedicine and Biomedical Technology, National Chi-Nan University, Taiwan.
[Ti] Título:Areca nut is associated with younger age of diagnosis, poor chemoradiotherapy response, and shorter overall survival in esophageal squamous cell carcinoma.
[So] Source:PLoS One;12(2):e0172752, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Areca nut chewing is carcinogenic to humans. However, little is known about the impact of areca nut chewing on esophageal squamous cell carcinoma (ESCC). METHODS: We retrospectively reviewed 286 ESCC patients who received surgery or preoperative chemoradiotherapy followed by surgery at our institution. Background characteristics including areca nut chewing history were analyzed. The 4-nitroquinoline 1-oxide (4-NQO)-induced murine ESCC model was used to test the impact of arecoline, a main constituent of areca nut, on ESCC. RESULTS: Compared to patients without areca nut chewing history, patients with areca nut chewing history had overall a younger age of onset (Mean age: 56.75 versus 52.68 yrs, P<0.001) and significantly worse overall survival than those without areca nut chewing history (P = 0.026). Among patients who received surgery, the overall survival rates were not significantly different between those with or without areca nut chewing history. Among patients who received preoperative chemoradiotherapy followed by surgery, those with areca nut chewing history had a significantly lower pathologic complete response rate (P = 0.002) and lower overall survival rate (P = 0.002) than those without. In the murine ESCC model, the incidence of esophageal invasive squamous cell carcinoma was 40% in mice exposed to concomitant 4-NQO and arecoline treatment for 8 weeks and 6% in mice exposed to 4-NQO only for 8 weeks (P = 0.037). CONCLUSIONS: Our results indicate that areca nut chewing history is significantly associated with younger age of onset, poor response to chemoradiotherapy, and shorter overall survival in ESCC patients. Arecoline, a main constituent of areca nut, accelerates esophageal tumorigenesis in the 4-NQO-induced murine ESCC model.
[Mh] Termos MeSH primário: Areca/efeitos adversos
Carcinoma de Células Escamosas/etiologia
Neoplasias Esofágicas/etiologia
Nozes/efeitos adversos
[Mh] Termos MeSH secundário: 4-Nitroquinolina-1-Óxido/toxicidade
Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Antineoplásicos/uso terapêutico
Arecolina/efeitos adversos
Carcinoma de Células Escamosas/induzido quimicamente
Carcinoma de Células Escamosas/mortalidade
Carcinoma de Células Escamosas/patologia
Neoplasias Esofágicas/induzido quimicamente
Neoplasias Esofágicas/mortalidade
Neoplasias Esofágicas/patologia
Feminino
Seres Humanos
Imuno-Histoquímica
Estimativa de Kaplan-Meier
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Meia-Idade
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 4ALN5933BH (Arecoline); 56-57-5 (4-Nitroquinoline-1-oxide)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170301
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0172752


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[PMID]:28019102
[Au] Autor:Dasgupta R; Chatterjee A; Sarkar S; Maiti BR
[Ad] Endereço:a Department of Zoology , University of Calcutta , Calcutta , India.
[Ti] Título:Arecoline aggravates hypothyroidism in metabolic stress in mice.
[So] Source:Arch Physiol Biochem;123(2):105-111, 2017 May.
[Is] ISSN:1744-4160
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Millions of people consume betel nut for increased capacity of work. It contains arecoline which is highly toxic and has several untoward side effects on endocrine functions. In this article, the role of arecoline on thyroid function under metabolic stress was investigated in mice. Water or food-deprivation, each for 5 days, caused ultrastructural degeneration of thyro-follicular cells, evident from pycnotic nuclei, scanty rough endoplasmic reticulum and mitochondria followed by depletion of blood serum T and T levels with alteration of TSH level as compared with control. Thyroid activity was also suppressed ultrastructurally as well as at hormonal level after arecoline administration. Further, arecoline treatment in water deprivation or food deprivation stress also caused thyroid dysfunction beyond that of metabolic stress, as evident from further ultrastructural degeneration of thyrocytes and depletion of thyroid hormones in mice. The findings suggest that arecoline aggravates hypothyroid condition in metabolic stress in mice.
[Mh] Termos MeSH primário: Arecolina/toxicidade
Agonistas Colinérgicos/toxicidade
Hipotireoidismo/induzido quimicamente
Hipotireoidismo/metabolismo
Estresse Fisiológico/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Hipotireoidismo/patologia
Masculino
Camundongos
Microscopia Eletrônica de Transmissão
Tireotropina/sangue
Tiroxina/sangue
Tri-Iodotironina/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholinergic Agonists); 06LU7C9H1V (Triiodothyronine); 4ALN5933BH (Arecoline); 9002-71-5 (Thyrotropin); Q51BO43MG4 (Thyroxine)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170314
[Lr] Data última revisão:
170314
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161227
[St] Status:MEDLINE
[do] DOI:10.1080/13813455.2016.1267228


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[PMID]:27648737
[Au] Autor:Hsieh CH; Hsu HH; Shibu MA; Day CH; Bau DT; Ho CC; Lin YM; Chen MC; Wang SH; Huang CY
[Ad] Endereço:Department of Health and Nutritional Biotechnology, Asia University, Taichung, Taiwan.
[Ti] Título:Down-regulation of ß-catenin and the associated migration ability by Taiwanin C in arecoline and 4-NQO-induced oral cancer cells via GSK-3ß activation.
[So] Source:Mol Carcinog;56(3):1055-1067, 2017 Mar.
[Is] ISSN:1098-2744
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cancer is one of the leading causes of death worldwide, and oral squamous cell carcinoma (OSCC) accounts for almost a sixth of all reported cancers. Arecoline, from areca nut is known to enhance carcinogenesis in oral squamous cells. The objective of this study is to determine the effect of Taiwanin C, from Taiwania cryptomerioides Hayata against Arecoline-associated carcinogenesis. An OSCC model was created in C57BL/6J Narl mice by administrating 0.5 mg mL arecoline with 0.2 mg mL 4-NQO carcinogen for 8 and 28 wk to mimic the etiology of oral cancer patients in Asia. Mice were sacrificed and two cell lines, T28 from the tumor and N28 cancerous cell line from the surrounding non tumor area, were established. Taiwanin C showed effective anti-tumor activity in nude mice models. Taiwanin C significantly inhibited the cell viability of T28 cells in a dose dependent manner, but did not inflict any effect on N28 normal cells. Taiwanin C treatment inhibited the migration ability of T28 cells in a dose dependent manner as determined by wound healing and migration assays. Taiwanin C also reduced the levels of ß-catenin and its downstream metastatic proteins, Tbx3 and c-Myc. Besides, Taiwanin C inhibited the nuclear accumulation of ß-catenin and induced ß-catenin degradation via proteasome-mediated pathway. Moreover, Taiwanin C enhanced GSK-3ß and reduced the p-ser GSK-3ß protein level to inactivate Wnt signaling. Taken together, Taiwanin C blocked the cell migration effects of T28 cells mediated through the activation of GSK-3ß to enhance protein degradation and reduce nuclear accumulation of ß-catenin. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Regulação para Baixo
Glicogênio Sintase Quinase 3 beta/metabolismo
Lactonas/administração & dosagem
Lignanas/administração & dosagem
Neoplasias Bucais/tratamento farmacológico
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: 4-Nitroquinolina-1-Óxido/efeitos adversos
Animais
Arecolina/efeitos adversos
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ativação Enzimática
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Lactonas/farmacologia
Lignanas/farmacologia
Camundongos
Neoplasias Bucais/induzido quimicamente
Neoplasias Bucais/metabolismo
Transdução de Sinais/efeitos dos fármacos
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CTNNB1 protein, human); 0 (Lactones); 0 (Lignans); 0 (beta Catenin); 0 (taiwanin C); 4ALN5933BH (Arecoline); 56-57-5 (4-Nitroquinoline-1-oxide); EC 2.7.11.1 (GSK3B protein, human); EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160921
[St] Status:MEDLINE
[do] DOI:10.1002/mc.22570


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[PMID]:26537528
[Au] Autor:Lin KH; Shibu MA; Kuo YH; Chen YC; Hsu HH; Bau DT; Chen MC; Tu CC; Viswanadha VP; Huang CY
[Ad] Endereço:Emergency Department, China Medical University Hospital, Taichung, Taiwan.
[Ti] Título:Taiwanin C selectively inhibits arecoline and 4-NQO-induced oral cancer cell proliferation via ERK1/2 inactivation.
[So] Source:Environ Toxicol;32(1):62-69, 2017 Jan.
[Is] ISSN:1522-7278
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Arecoline, the most abundant alkaloid in betel nut is known to promote abnormal proliferation of epithelial cells by enhancing epidermal growth factor receptor (EGFR) activation and cyclooxygenase-2 (COX2) expression. Taiwanin C, a naturally occurring lignan extracted from Taiwania cryptomerioides, has been found to be a potential inhibitor of COX2 expression. Based on the MTT assay results, taiwanin C was found to be effective in inhibiting the tumorous T28 cell than the non-tumorous N28 cells. The modulations in the expression of relevant proteins were determined to understand the mechanism induced by taiwanin C to inhibit T28 cell proliferation. The levels of activated EGFR and COX2 were found to be abnormally high in the T28 oral cancer cells. However, taiwanin C was found to inhibit the activation of EGFR and regulated other related downstream proteins and thereby inhibited the T28 cell proliferation. In conclusion the results indicate that taiwanin C suppresses COX2-EGFR and enhances P27 pathways to suppress arecoline induced oral cancer cell proliferation via ERK1/2 inactivation. © 2015 Wiley Periodicals, Inc. Environ Toxicol 32: 62-69, 2017.
[Mh] Termos MeSH primário: 4-Nitroquinolina-1-Óxido/toxicidade
Antineoplásicos Fitogênicos/farmacologia
Arecolina/antagonistas & inibidores
Arecolina/toxicidade
Proliferação Celular/efeitos dos fármacos
Inibidores de Ciclo-Oxigenase 2/farmacologia
Lactonas/farmacologia
Lignanas/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Neoplasias Bucais/patologia
[Mh] Termos MeSH secundário: Animais
Proteínas de Ciclo Celular/antagonistas & inibidores
Proteínas de Ciclo Celular/biossíntese
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Receptor do Fator de Crescimento Epidérmico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Cell Cycle Proteins); 0 (Cyclooxygenase 2 Inhibitors); 0 (Lactones); 0 (Lignans); 0 (taiwanin C); 4ALN5933BH (Arecoline); 56-57-5 (4-Nitroquinoline-1-oxide); EC 2.7.10.1 (EGFR protein, mouse); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151106
[St] Status:MEDLINE
[do] DOI:10.1002/tox.22212


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[PMID]:27405178
[Au] Autor:Huang XT; Xiao RM; Wang MF; Wang JJ; Chen Y
[Ti] Título:[Induction of rat hepatic CYP2E1 expression by arecoline in vivo].
[So] Source:Yao Xue Xue Bao;51(1):153-6, 2016 Jan.
[Is] ISSN:0513-4870
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:The regulation mechanism of arecoline on rat hepatic CYP2E1 was studied in vivo. After oral administration of arecoline hydrobromide (AH; 4, 20 and 100 mg x kg(-1) x d(-1)) to rats for one week, the hepatic CYP2E1 mRNA level remained unchanged, but the hepatic CYP2E1 protein content was dose-dependently increased. Additionally, although the hepatic CYP2E1 activity was induced by AH treatment, the induction was attenuated with the increase in dosage. The results indicate that the effect of arecoline on rat hepaticdoes not involve transcriptional activation of the gene, but largely involves the stabilization of CYP2E1 protein against degradation or increased efficiency of CYP2E1 mRNA translation, and additionally involve the post- ranslational modification of CYP2E1 protein. Furthermore, the CYP2E1 response is fairly equal among the different species, the induction of rat hepatic CYP2E1 by arecoline suggests that there is a risk of metabolic interaction among the substrate drugs of CYP2E1 in betel-quid use human.
[Mh] Termos MeSH primário: Arecolina/farmacologia
Indutores do Citocromo P-450 CYP2E1/farmacologia
Citocromo P-450 CYP2E1/metabolismo
Fígado/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Fígado/metabolismo
RNA Mensageiro
Ratos
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytochrome P-450 CYP2E1 Inducers); 0 (RNA, Messenger); 4ALN5933BH (Arecoline); EC 1.14.13.- (Cytochrome P-450 CYP2E1)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:160713
[Lr] Data última revisão:
160713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160714
[St] Status:MEDLINE


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[PMID]:27393441
[Au] Autor:Yu H; Tang L; Wu H; Wang K; Cai B; Zhang X; Zhang C; Yin Y
[Ad] Endereço:School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, China / Jiangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Medical, Nanjing University of Chinese Medicine, Nanjing, China / Engineering Center of State Ministry of Education for Standardization of Chinese Med
[Ti] Título:Determination of contents of four alkaloids in Pericarpium arecae by quantitative analysis of multi-components by single-marker.
[So] Source:Pak J Pharm Sci;29(4):1269-74, 2016 Jul.
[Is] ISSN:1011-601X
[Cp] País de publicação:Pakistan
[La] Idioma:eng
[Ab] Resumo:By using a typical component in traditional Chinese medicine Pericarpium Arecae (PA), quantitative analysis of multi-components by single-marker (QAMS) was performed to determine the contents of four alkaloids. With a column packed with strong cation exchange bonded silica particles, the alkaloids were well separated, showing linear relationships within certain ranges. The limit of detection, limit of quantitation, precision, stability, repeatability and recovery all met requirements. By employing arecoline as internal standard, relative correction factors for arecaidine, guvacine and guvacoline at five concentrations were detected with three HPLC systems and three HPLC columns. The peaks of arecaidine, guvacine and guvacoline were positioned, during which the columns with the same packing materials from different manufacturers significantly affected relative retention values and retention time differences of the alkaloids. However, the columns, from different batches, managed to give relative retention values satisfying the requirements of HPLC peak positioning. The Thermo Fisher Scientific column packed with strong cation exchange bonded silica particles was finally selected by considering resolution and peak time. Compared with the external standard method, QAMS detected the alkaloid contents in 12 PA samples more accurately and reliably. The results provide valuable evidence for content determination and quality control of alkaloids in PA.
[Mh] Termos MeSH primário: Alcaloides/análise
Areca/química
Cromatografia Líquida de Alta Pressão/métodos
[Mh] Termos MeSH secundário: Arecolina/análogos & derivados
Arecolina/análise
Limite de Detecção
Ácidos Nicotínicos/análise
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Alkaloids); 0 (Nicotinic Acids); 0 (guvacoline); 0S8YEV0D4O (arecaidine); 41538P325K (guvacine); 4ALN5933BH (Arecoline)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:160709
[Lr] Data última revisão:
160709
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160710
[St] Status:MEDLINE


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[PMID]:27260964
[Au] Autor:Persyn S; De Wachter S; Wyndaele JJ; Eastham J; Gillespie J
[Ad] Endereço:Department of Urology, Antwerp University Hospital and University of Antwerp, Faculty of Medicine, Antwerp, Belgium. Electronic address: sarapersyn@hotmail.com.
[Ti] Título:The actions of isoprenaline and mirabegron in the isolated whole rat and guinea pig bladder.
[So] Source:Auton Neurosci;198:19-27, 2016 Jul.
[Is] ISSN:1872-7484
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:ß3-adrenoceptor agonists influence overactive bladder in humans and animal models. However, data is emerging that the mode of action of these drugs is complex. The present study explored the actions of the ß3-adrenergic agonist mirabegron and the non-selective agonist isoprenaline on the contractile systems in the rat and guinea pig bladder. Intravesical pressure was measured in isolated whole bladders from female adult animals. In both species spontaneous contractile activity was observed. The muscarinic agonist arecaidine produced complex responses consisting of an initial transient pressure rise followed by complex phasic activity. Three contractile elements were identified: intrinsic micro-contractile activity, initial transient response and steady state phasic activity. The intrinsic and steady state activity could be further divided into a baseline pressure with superimposed phasic activity. The effects of isoprenaline and mirabegron were investigated on these elements. In the rat, the micro-contractile activity could be completely inhibited by isoprenaline (full agonist). The arecaidine-induced initial and steady state baseline pressures were partially reduced, while the phasic activity was little affected. In the guinea pig, both the arecaidine-induced baseline pressure and the phasic activity were affected by isoprenaline. Mirabegron didn't produce significant inhibitory effects in any of the contractile elements in either species. These results show that complex contractile systems operate in the rat and guinea pig bladder that can be modulated by ß1/ß2-adrenoceptor mechanisms. No evidence was obtained for any ß3-dependent regulation of contraction. These data support similar data in humans. Therefore the primary site of therapeutic action of ß3-adrenergic agonists remains unknown.
[Mh] Termos MeSH primário: Acetanilidas/farmacologia
Isoproterenol/farmacologia
Contração Muscular/efeitos dos fármacos
Tiazóis/farmacologia
Bexiga Urinária/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Arecolina/análogos & derivados
Arecolina/farmacologia
Carbacol/farmacologia
Feminino
Cobaias
Técnicas In Vitro/métodos
Agonistas Muscarínicos/farmacologia
Contração Muscular/fisiologia
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetanilides); 0 (Muscarinic Agonists); 0 (Thiazoles); 0S8YEV0D4O (arecaidine); 4ALN5933BH (Arecoline); 8Y164V895Y (Carbachol); L628TT009W (Isoproterenol); MVR3JL3B2V (mirabegron)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160605
[St] Status:MEDLINE


  9 / 878 MEDLINE  
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[PMID]:27255601
[Au] Autor:Jiang JM; Wang L; Gu HF; Wu K; Xiao F; Chen Y; Guo RM; Tang XQ
[Ad] Endereço:Department of Cardiology, The Affiliated Hospital, Guangdong Medical University, 57 W Friendship Street People Avenue South, Zhanjiang, 524001, Guangdong, People's Republic of China.
[Ti] Título:Arecoline Induces Neurotoxicity to PC12 Cells: Involvement in ER Stress and Disturbance of Endogenous H2S Generation.
[So] Source:Neurochem Res;41(8):2140-8, 2016 Aug.
[Is] ISSN:1573-6903
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Arecoline is a major alkaloid of areca nut and has been effect on central nervous system. Although arecoline-induced neurotoxicity has been reported, the possible underlying neurotoxic mechanisms have not yet been elucidated. Increasing evidences have shown that both excessive endoplasmic reticulum (ER) stress and disturbance of hydrogen sulfide (H2S) production are involved in the pathophysiology of numerous neurodegenerative diseases. Here, the purpose of present study was to verify whether ER stress and the disturbance of endogenous H2S generation are also involved in arecoline-caused neurotoxicity. We found that treatment of PC12 cells with arecoline induced the down-regulation of cells viability and up-regulation of apoptosis and the activity of caspase-3, indicating the neurotoxic role of arecoline to PC12 cells. In addition, arecoline also increased the expression of Bax (pro-apoptotic protein) and attenuated the expression of Bcl-2 (anti-apoptotic protein) in PC12 cells. Simultaneously, arecoline caused excessive ER stress in PC12 cells, as evidenced by the up-regulations of Glucose-regulated protein 78 (GRP78), CCAAT/enhancer binding protein homologous protein (CHOP), and Cleaved caspase-12 expressions. Notably, the level of H2S in the culture supernatant and the expressions of cystathionine ß-synthase and 3-mercaptopyruvate sulfurtransferase (two major enzymes for endogenous H2S generation in PC12 cells) were also reduced by arecoline treatment. These results indicate that arecoline-caused neurotoxicity to PC12 cells is involved in ER stress and disturbance of endogenous H2S generation and suggest that the modulation of ER stress and endogenous H2S generation may be potential therapeutic approach in treatment of arecoline-caused neurotoxicity.
[Mh] Termos MeSH primário: Arecolina/toxicidade
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Estresse do Retículo Endoplasmático/fisiologia
Sulfeto de Hidrogênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/fisiologia
Relação Dose-Resposta a Droga
Células PC12
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
4ALN5933BH (Arecoline); YY9FVM7NSN (Hydrogen Sulfide)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160604
[St] Status:MEDLINE
[do] DOI:10.1007/s11064-016-1929-6


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Fotocópia
[PMID]:27046150
[Au] Autor:Liu YJ; Peng W; Hu MB; Xu M; Wu CJ
[Ad] Endereço:a College of Pharmacy , Chengdu University of Traditional Chinese Medicine , Chengdu , PR China.
[Ti] Título:The pharmacology, toxicology and potential applications of arecoline: a review.
[So] Source:Pharm Biol;54(11):2753-2760, 2016 Nov.
[Is] ISSN:1744-5116
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:CONTEXT: Arecoline is an effective constituent of Areca catechu L. (Arecaceae) with various pharmacological effects. However, investigations also revealed that long use of arecoline could arouse some oral diseases. OBJECTIVE: The present review gathers the fragmented information available in the literature (before 1 October 2015) regarding pharmacology and toxicology of arecoline. We also discussed the potential developments and applications of arecoline in the future. METHODS: All the available information regarding the arecoline is compiled from scientific databases, including Science Direct, PubMed, Web of Science, Scopus, etc. RESULTS: Previous research demonstrated that arecoline is one of the major effective constituents in A. catechu. Additionally, arecoline has a wide spectrum of pharmacological activities including effects on nervous, cardiovascular, digestive and endocrine systems and anti-parasitic effects. What's more, arecoline is reported to be the primary toxic constituent of A. catechu, and the main toxic effects include oral submucous fibrosis (OSF), oral squamous cell carcinoma (OSCC) and genotoxicity. CONCLUSION: Arecoline has great potential to be a therapeutic drug for various ailments. However, further investigations are needed in the future to reduce or eliminate its toxicities before developing into new drug.
[Mh] Termos MeSH primário: Arecolina/farmacologia
[Mh] Termos MeSH secundário: Animais
Arecolina/uso terapêutico
Arecolina/toxicidade
Sistema Cardiovascular/efeitos dos fármacos
Glândulas Endócrinas/efeitos dos fármacos
Seres Humanos
Sistema Nervoso/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
4ALN5933BH (Arecoline)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170207
[Lr] Data última revisão:
170207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160406
[St] Status:MEDLINE



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