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.

The origin of the hypertensive effect of arecoline in rats.

Abstract: Arecoline, injected intravenously in rats, causes a short-lasting hypotension followed by a hypertension of long duration. The hypertensive effect of arecoline results mainly from its stimulating acti

Synthetic or Imitation Nicotine Compositions, Processes and Methods of Manufacture

Abstract: Processes and methods of manufacturing a synthetic or imitation nicotine product are provided. One process may include the steps of providing a plurality of areca fruits, drying the plurality of areca fruits, dehusking the plurality of areca fruits to obtain a plurality of areca nuts, chopping, shredding or grinding the plurality of areca nuts into a multiplicity of areca nut particles, introducing the multiplicity of areca nut particles into a tank containing water, agitating the multiplicity of areca nut particles to create a slurry, determining an amount of arecoline in the slurry and pumping the water having the predetermined amount of arecoline through a filter and into a holding tank and evaporating the arecoline from the water. An imitation nicotine product that may include 1% to 20% arecoline by weight with other elements may then be manufactured.

Arecoline, Hesperidin and Trifluoperazine-mediated Cytotoxicity and Cell Death Potential in NIH/3T3 Fibroblasts Cells –Toxicity/Safety Assessment in a NIH/3T3 Model Fibroblast Cell Line

Abstract: Aim/Background: Arecoline is considered to be the principal etiologic agent for Oral Sub mucous Fibrosis (OSF) with the buccal fibroblasts being the major target. Hence, this model alkaloid has been used to evaluate toxicity and cell death potential in NIH/3T3 cells and compared with that of Hesperidin. Materials and Methods: Toxicity and cell death, for the two molecules, was tested using a battery of assays (MTT assay based cytotoxicity assessment; AO/EtBr assay-based determination of the percentage of dead cells; PI-based cell-cycle and cell death analysis using flow cytometry; DCFH-DA-based ROS levels). We also evaluated the role of S100A4 in this process using Trifluoperazine (TFP)an antagonist of this protein. These experiments involved challenging the cells with arecoline and protecting them with Hesperidin and TFP separately. Results: IC50 measurements, based on the MTT assay, were found to be 38μM and 7. 5 Micromolar respectively. Based on the AO/EtBr and the flow cytometry assay, both the chemicals exhibited a dose-dependent increase in cell death. Both chemicals arrested the cells in different phases of the cell cycle. Arecoline and Hesperidin altered ROS levels in a dosedependent manner. Our challenge-protection experiments showed that Hesperidin and TFP, were able to reduce the arecoline-mediated cell death in NIH/3T3 fibroblasts. These results may due to an alteration in the ROS levels, despite quantitative differences in their cytotoxicity and cell death potential. The protection-challenge experiments showed that Arecoline and TFP may have a marginal cytoprotective effect. Conclusions: Our results substantiates and validates our experimental design to evaluate the toxicity and safety of model fibrotic chemicals as well as test the probable protective effects conferred by Hesperidin-like natural molecules as well as possibly address mechanistic issues pertaining to ROS as well as S100A4 antagonism using TFP and related molecules.

Regulatory effects of chronically repeated nicotine treatment towards the functions of central muscarinic receptors

Abstract: In rats, nicotine was subcutaneously injected at the dose of 2.0 mg·kg 1 twice a day for 10 d, the chronic tolerance to the effects of nicotine for producing hypothermia, disability of rotarod performance, behavioral convulsions was developed, the threshold dose of muscarinic receptor agonist arecoline for producing electroencephalogram seizures was decreased. In addition, rats were treated with nicotine 2.0 or/and arecoline 5.0 mg·kg 1 ip twice a day for 14 d, the down regulation of cerebral muscarinic receptors was produced by the combination of nicotine with arecoline, which could be prevented by nicotinic receptor antagonist mecamylamine 1.0 mg·kg 1 . It is suggested that the sensitivity of muscarinic receptors to the agonist arecoline for producing electroencephalogram seizures and its receptor down regulative effect is increased by chronically repeated nicotine treatment in rats.