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.

Study on the Caspase-3 Activity in the Arecoline-induced Apoptosis of Endothelial Cells.

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.

Arecoline induces dual modulation of blood pressure in rat, including an initial downregulation and a subsequent upregulation

Abstract: Purpose: To determine the role of arecoline in cardiovascular modulation in rats.Methods: After rats were anaesthetized with intraperitoneal urethane (1.4 g/kg body weight), saline or arecoline (at doses of 1.0, 3.0 and 10.0 mg/kg) was intraperitoneally administered, and blood pressure (BP) was continuously recorded using a physiological apparatus. Mean arterial pressure (MAP), maximum changes in MAP and reaction time due to arecoline stimulations were calculated and analyzed.Results: Arecoline induced biphasic modulation in BP, including an initial downregulation followed by a subsequent upregulation. The MAP and maximum change in MAP exhibited a concentration-dependent effect in the downregulation phase (p 0.05 within each group), while BP reaction time showed a dose-dependent prolongation in both downregulation and upregulation phases (ps < 0.01 within each group). Remarkably, arecoline-induced BP downregulation more rapidly and drastically than upregulation in each arecoline group.Conclusion: These results indicate that arecoline exerts a complex effect in cardiovascular modulation that should be considered as side effects in the clinical use of arecoline and/or with the habitual chewing of areca nuts. Keywords: Arecoline, Blood pressure, Downregulation, Upregulation

Improvement of autophagic flux mediates the protection of hydrogen sulfide against arecoline-elicited neurotoxicity in PC12 cells

Abstract: ABSTRACT Arecoline, the most abundant alkaloid of the areca nut, induces toxicity to neurons. Hydrogen sulfide (H2S) is an endogenous gas with neuroprotective effects. We recently found that arecoline reduced endogenous H2S content in PC12 cells. In addition, exogenously administration of H2S alleviated the neurotoxicity of arecoline on PC12 cells. Increasing evidence has demonstrated the neuroprotective role of improvement of autophagic flux. Therefore, the aim of the present work is to explore whether improvement of autophagic flux mediates the protection of H2S against arecoline-caused neurotoxicity. Transmission electron microscope (TEM) for observation of ultrastructural morphology. Western blotting was used to detect protein expression of the related markers. Functional analysis contained LDH release assay, Hoechst 33,258 nuclear staining and flow cytometry were used to detect cytotoxicity and apoptosis. In the present work, we found that arecoline disrupted autophagy flux in PC12 cells as evidenced by accumulation of autophagic vacuoles, increase in LC3II/LC3I, and upregulation of p62 expression in PC12 cells. Notably, we found that sodium hydrosulfide (NaHS), the donor of H2S improved arecoline-blocked autophagy flux in PC12 cells. Furthermore, we found that blocking autophagic flux by chloroquine (CQ), the inhibitor of autophagy flux, antagonized the inhibitory role of NaHS in arecoline-induced cytotoxicity apoptosis and endoplasmic reticulum (ER) stress. In conclusion, H2S improves arecoline-caused disruption of autophagic flux to exert its protection against the neurotoxicity of arecoline.