Quinone Reductase Inducing Activity of the Dichloromethane/Ethanol Extract of the Roots of Pulsatilla Chinensis

Agents with phase II enzyme inducing activities play important roles in intervening in the carcinogenic process. In the present study, the quinone reductase (QR) inducing activities of nine known triterpene saponins from the dichloromethane/ethanol extract of the roots of Pulsatilla chinensis were tested. The oleanane saponins exhibited more potent QR inducing activities than the lupane saponins, and the CD value of the compound with the most potent QR inducing activity was 1.1 μM. The chemopreventive activity of the dichloromethane/ethanol extract was also evaluated using the DMBA-induced mice model.

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Activity-Guided Isolation of Constituents ofRenealmianicolaioideswith the Potential to Induce the Phase II Enzyme Quinone Reductase

Journal of Natural Products ◽

10.1021/np020249p ◽

2002 ◽

Vol 65 (11) ◽

pp. 1616-1620 ◽

Cited By ~ 36

Author(s):

Jian-Qiao Gu ◽

Eun Jung Park ◽

Jose Schunke Vigo ◽

James G. Graham ◽

Harry H. S. Fong ◽

...

Keyword(s):

Phase Ii ◽

Quinone Reductase ◽

Phase Ii Enzyme

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In Vitro and in Vivo Regulation of Antioxidant Response Element-Dependent Gene Expression by Estrogens

Endocrinology ◽

10.1210/en.2003-0817 ◽

2004 ◽

Vol 145 (1) ◽

pp. 311-317 ◽

Cited By ~ 51

Author(s):

P. J. Ansell ◽

C. Espinosa-Nicholas ◽

E. M. Curran ◽

B. M. Judy ◽

B. J. Philips ◽

...

Keyword(s):

Gene Expression ◽

Phase Ii ◽

Enzyme Activities ◽

Antioxidant Response ◽

Quinone Reductase ◽

Antioxidant Response Element ◽

Phase Ii Enzyme ◽

17Β Estradiol

Abstract Understanding estrogen’s regulation of phase II detoxification enzymes is important in explaining how estrogen exposure increases the risk of developing certain cancers. Phase II enzymes such as glutathione-S-transferases (GST) and quinone reductase protect against developing chemically induced cancers by metabolizing reactive oxygen species. Phase II enzyme expression is regulated by a cis-acting DNA sequence, the antioxidant response element (ARE). It has previously been reported that several antiestrogens, but not 17β-estradiol, could regulate ARE-mediated gene transcription. Our goal was to determine whether additional estrogenic compounds could regulate ARE-mediated gene expression both in vitro and in vivo. We discovered that physiological concentrations (10 nm) of 17β-estradiol repressed GST Ya ARE-dependent gene expression in vitro. Treatment with other endogenous and anti-, xeno-, and phytoestrogens showed that estrogen receptor/ARE signaling is ligand, receptor subtype, and cell type specific. Additionally, GST and quinone reductase activities were significantly lowered in a dose-dependent manner after 17β-estradiol exposure in the uteri of mice. In conclusion, we have shown that 17β-estradiol, and other estrogens, down-regulate phase II enzyme activities. We propose estrogen-mediated repression of phase II enzyme activities may increase cellular oxidative DNA damage that ultimately can result in the formation of cancer in some estrogen-responsive tissues.

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