Pharmacokinetic Study in Mice of Galphimine-A, an Anxiolytic Compound from Galphimia glauca

Molecules

Rodolfo Abarca Vargas¹  Alejandro Zamilpa¹  Francisco Alarcón Aguilar²  Maribel Herrera-Ruiz¹  Jaime Tortoriello¹ 

[1] Centro de Investigación Biomédica del Sur, Instituto Mexicano del Seguro Social (IMSS), Argentina No. 1, Col. Centro, Xochitepec 62790, Morelos, Mexico; E-Mails:;Doctorado en Ciencias Biológicas y de la Salud, División de Ciencias Biológicas y de la Salud, Universidad Autónoma Metropolitana-Iztapalapa, San Rafael Actlixco No. 186, Col. Vicentina, Iztapalapa 09340, Mexico; E-Mail:

关键词: Galphimia glauca;    pharmacokinetics;    phytopharmaceutical;    galphimine-A;    anxiety;   

DOI  :  10.3390/molecules19033120

来源: mdpi

【 摘 要 】

The aim of this study was to obtain pharmacokinetic data for the anxiolytic compound galphimine-A (G–A) from Galphimia glauca. G–A is the most abundant anxiolytic compound in this plant, while Galphimine-E (G–E) is the most abundant galphimine, but inactive. G–E was transformed chemically into G–A. The pharmacokinetic study was carried out in ICR mice, which were orally administered a single 200 mg/kg dose of G–A. Samples of blood and brain were taken at different times after administration of G–A. Previously, we established the validation of methods for determining the concentration of G–A. The G–A was detected in plasma 5 min after oral administration, and its concentration reached 2.47 μg/mL. Data from concentration-time curves allowed us to establish the main pharmacokinetic parameters in two models: one- and/or two-compartment. C_max values were 3.33 and 3.42 μg/mL respectively, likewise AUC_{0→1440 min} were 1,951.58 and 1,824.95 μg/mL·min. The G–A in brain tissue was noted to cross the blood-brain barrier, reaching C_max 2.74 μg/mL, T_max 81.6 min, and then drop gradually to 0.32 μg/mL detected at 24 h. The presence of G–A in brain tissue, confirmed that this anxiolytic compound can access the target organ and acts directly on the CNS.

【 授权许可】

CC BY   
© 2014 by the authors; licensee MDPI, Basel, Switzerland.