Ineffectiveness of American ginseng in the prevention of dimethylbenzanthracene-induced mammary tumors in mice.
The potential of American ginseng (AG) ( Panax quinquefolium), a commonly used herbal remedy believed to have anticarcinogenic effects, to prevent the development of mammary tumors was evaluated in a mouse model of dimethylbenzanthracene (DMBA)-induced mammary carcinoma. Ginsenosides, believed to be the active components of ginseng and that have a chemical structure similar to estradiol, have previously been shown to possess phytoestrogen-like qualities similar to the soy isoflavone genistein. The effects of AG, administered as powdered root, were compared to the selective estrogen receptor modulators tamoxifen and ospemifene. Eighty-three female SENCAR mice were divided into four treatment groups: control (N = 23), AG (N = 20), ospemifene (N = 20), and tamoxifen (N = 20). American ginseng, ospemifene, and tamoxifen were administered at a dose of 50 mg/kg/day orally by gavage, with the control mice receiving vehicle only. For the first 6 weeks, all mice received 20 microg/day DMBA in combination with their respective treatments. DMBA was then withdrawn, and daily treatments continued for a total of approximately 52 weeks. As expected, ospemifene (p = 0.01) and tamoxifen (p = 0.004) significantly reduced the incidence of mammary tumors compared to the control mice, which had a mammary tumor incidence of approximately 57%. The incidence of mammary carcinomas in the AG group was 40%, a reduction of approximately 29% compared to control. These results suggest that AG may still have the potential to prevent the development of mammary tumors in a chemically induced breast cancer mouse model, although the present study showed no significant difference between control and AG-treated mice.
Wurz
Gregory T
GT
Department of Internal Medicine, Division of Hematology and Oncology, Cancer Center, The University of California, Davis, Sacramento 95817, USA.
Marchisano-Karpman
Cristina
C
DeGregorio
Michael W
MW
D015127:9,10-Dimethyl-1,2-benzanthracene; D000818:Animals; D016588:Anticarcinogenic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D002471:Cell Transformation, Neoplastic / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D005260:Female; D008325:Mammary Neoplasms, Experimental / Q000737:chemistry / Q000517:prevention & control*; D051379:Mice; D018632:Mice, Inbred SENCAR; D005894:Panax; D008517:Phytotherapy; D028321:Plant Preparations / Q000494:pharmacology* / Q000627:therapeutic use; D018517:Plant Roots; D020845:Selective Estrogen Receptor Modulators / Q000494:pharmacology* / Q000627:therapeutic use; D013629:Tamoxifen / Q000031:analogs & derivatives / Q000494:pharmacology; D013997:Time Factors
D016588:Anticarcinogenic Agents; D028321:Plant Preparations; D020845:Selective Estrogen Receptor Modulators; D013629:Tamoxifen; D015127:9,10-Dimethyl-1,2-benzanthracene; C119141:Ospemifene