A Strong Protective Action of Guttiferone-A, a Naturally Occurring Prenylated Benzophenone, Against Iron-Induced Neuronal Cell Damage

Journal of Pharmacological Sciences

Zeki Naal³  Laura García-Pupo²  Osmany Cuesta Rubio¹  Yanier Núñez Figueredo²  Carlos Curti³  Gilberto L. Pardo Andreu⁴  René Delgado Hernández² 

[1] Departamento de Farmacia, Instituto de Farmacia y Alimentos, Universidad de La Habana, Cuba;Laboratorio de Farmacología Molecular, Centro de Investigación y Desarrollo de Medicamentos, Cuba;Departamento de Física e Química, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Brazil;Centro de Estudio para las Investigaciones y Evaluaciones Biológicas, Instituto de Farmacia y Alimentos, Universidad de La Habana, Cuba

关键词: guttiferone-A;    iron;    neuroprotection;    antioxidant;    iron chelation;   

DOI  :  10.1254/jphs.10273FP

学科分类：药学

来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society

【 摘 要 】

References(50)Cited-By(6)Guttiferone-A (GA) is a natural occurring polyisoprenylated benzophenone with several reported pharmacological actions. We have assessed the protective action of GA on iron-induced neuronal cell damage by employing the PC12 cell line and primary culture of rat cortical neurons (PCRCN). A strong protection by GA, assessed by the 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carbox-anilide (XTT) assay, was revealed, with IC50 values <1 μM. GA also inhibited Fe3+–ascorbate reduction, iron-induced oxidative degradation of 2-deoxiribose, and iron-induced lipid peroxidation in rat brain homogenate, as well as stimulated oxygen consumption by Fe2+ autoxidation. Absorption spectra and cyclic voltammograms of GA–Fe2+/Fe3+ complexes suggest the formation of a transient charge transfer complex between Fe2+ and GA, accelerating Fe2+ oxidation. The more stable Fe3+ complex with GA would be unable to participate in Fenton-Haber Weiss-type reactions and the propagation phase of lipid peroxidation. The results show a potential of GA against neuronal diseases associated with iron-induced oxidative stress.

【 授权许可】

Unknown