Study on estrogenic effect of genistein and apigenin in vitro / 中国中药杂志
China Journal of Chinese Materia Medica
;
(24): 2317-2322, 2012.
Artigo
em Chinês
| WPRIM
| ID: wpr-263934
ABSTRACT
<p><b>OBJECTIVE</b>To detect the estrogenic activity of genistein and apigenin with ER-positive cell line MCF-7 human breast cancer cells.</p><p><b>METHOD</b>MTT method was adopted to study the impact of genistein and apigenin on MCF-7 proliferation in vitro. Real-time RT-PCR method was used to detect their impact on ERalpha, ERbeta, PR and PS2 mRNA expression levels.</p><p><b>RESULT</b>Genistein and apigenin promoted the proliferation of MCF-7. Genistein 1 x 10(-10) mol x L(-1) group showed a significant increase in the expression of ERa mRNA levels or a 17. 76 times more than the control group and a 1.75 times more than the E2 group. Apigenin notably promoted the PR mRNA expression or a 4. 57 times more than the control group and a 1.11 times more than the E2 group. Both of them had different effect in promoting ERalpha, ERbeta, PR or PS2 mRNA.</p><p><b>CONCLUSION</b>Both genistein and apigenin have a strong estrogen-like effect. Although they have different effect in promoting estrogenic response genes (such as ERa, ERbeta, PR and PS2 mRNA), genistein shows a stronger activity than apigenin. It also suggests that the signaling pathways of phytoestrogens showing estrogen-like effect are not completely identical with estrogen pathways. The B-cycle position of flavonoids is one of the key sites to estrogen-like activity, and isoflavones (cycle B on site 3) show stronger estrogen-like activity than flavones (B-cycle lies in site 2).</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Farmacologia
/
Expressão Gênica
/
Genisteína
/
Apigenina
/
Receptor alfa de Estrogênio
/
Receptor beta de Estrogênio
/
Fitoestrógenos
/
Proliferação de Células
/
Presenilina-2
/
Células MCF-7
Limite:
Feminino
/
Humanos
Idioma:
Chinês
Revista:
China Journal of Chinese Materia Medica
Ano de publicação:
2012
Tipo de documento:
Artigo
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