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Pharmacological and biological screening of ascorbigen: protection against glucose‐induced endothelial cell toxicity
Author(s) -
Joshi Mandar S.,
Bauer John A.,
Werbovetz Karl A.,
Barszcz Todd,
Patil Popat N.
Publication year - 2008
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.2494
Subject(s) - pharmacology , nitric oxide , toxicity , biological activity , chemistry , histamine , mechanism of action , phenylephrine , biochemistry , biology , in vitro , endocrinology , organic chemistry , blood pressure
Cruciferous vegetables contain significant amounts of ascorbigen and related substances with known molecular structures. This study tested the hypothesis that ascorbigen demonstrates antioxidant properties and protects human umbilical cord endothelial cells against hyperglycemic toxicity in vitro . It was observed that ascorbigen, in micromolar concentrations, protected against endothelial cell death from glucose toxicity. Additionally, ascorbigen at 3.0 mm shifted the concentration response curve of l‐phenylephrine to the right, with a reduction in the maximal contractile effects of the agonist. This action was not related to α ‐adrenoceptor blockade. Ascorbigen also relaxed the vascular tone induced by l‐phenylephrine, which is not mediated by an endothelial cell nitric oxide‐dependent mechanism. On the guinea‐pig ileum, the spasmogenic effects of carbachol, histamine and serotonin were reduced in the presence of 3 m m ascorbigen. Spasm of the gut induced by the acetylcholinesterase inhibitor, physostigmine, was antagonized by ascorbigen with an IC50 of 286 µ m . This natural product also has a weak antiparasitic activity. The cytoprotective effects of ascorbigen may be highly relevant in the optimum physiological regulation of the function and the therapeutic value of this substance in disease settings needs to be further investigated. Copyright © 2008 John Wiley & Sons, Ltd.