Abstract Title:

Polyphenolic compounds from Artemisia dracunculus L. inhibit PEPCK gene expression and gluconeogenesis in an H4IIE hepatoma cell line.

Abstract Source:

Am J Physiol Endocrinol Metab. 2007 Dec;293(6):E1503-10. Epub 2007 Sep 11. PMID: 17848630

Abstract Author(s):

Dmitry Govorko, Sithes Logendra, Yanxin Wang, Debora Esposito, Slavko Komarnytsky, David Ribnicky, Alexander Poulev, Zhong Wang, William T Cefalu, Ilya Raskin

Article Affiliation:

Rutgers University, Biotech Center, 59 Dudley Road, New Brunswick, NJ 08901, USA. [email protected]


An ethanolic extract of Russian tarragon, Artemisia dracunculus L., with antihyperglycemic activity in animal models was reported to decrease phosphoenolpyruvate carboxykinase (PEPCK) mRNA expression in STZ-induced diabetic rats. A quantitative polymerase chain reaction (qPCR) assay was developed for the bioactivity-guided purification of the compounds within the extract that decrease PEPCK expression. The assay was based on the inhibition of dexamethasone-stimulated PEPCK upregulation in an H4IIE hepatoma cell line. Two polyphenolic compounds that inhibited PEPCK mRNA levels were isolated and identified as 6-demethoxycapillarisin and 2',4'-dihydroxy-4-methoxydihydrochalcone with IC(50) values of 43 and 61 muM, respectively. The phosphoinositide-3 kinase (PI3K) inhibitor LY-294002 showed that 6-demethoxycapillarisin exerts its effect through the activation of the PI3K pathway, similarly to insulin. The effect of 2',4'-dihydroxy-4-methoxydihydrochalcone is not regulated by PI3K and dependent on activation of AMPK pathway. These results indicate that the isolated compounds may be responsible for much of the glucose-lowering activity of the Artemisia dracunculus extract.

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