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Black Cohosh: Insights into its Mechanism(s) of Action.

Ruhlen RL, Sun GY, Sauter ER - Integr Med Insights (2008)

Bottom Line: Although the mechanism by which BCE relieves symptoms is unknown, several hypotheses have been proposed: it acts 1) as a selective estrogen receptor modulator, 2) through serotonergic pathways, 3) as an antioxidant, or 4) on inflammatory pathways.We found that while the most prominent triterpene in BCE, 23-epi-26-deoxyactein, suppresses cytokine-induced nitric oxide production in brain microglial cells, the whole BCE extract actually enhanced this pathway.A variety of activities have been reported for black cohosh and its compounds, but the absorption and tissue distribution of these compounds is unknown.

View Article: PubMed Central - PubMed

Affiliation: Departments of Surgery and.

ABSTRACT
The Women's Health Initiative found that combination estrogen and progesterone hormone replacement therapy increases breast cancer and cardiovascular disease risk, which compelled many women to seek herbal alternatives such as black cohosh extract (BCE) to relieve their menopausal symptoms. While several clinical trials document the efficacy of BCE in alleviating menopausal symptoms, preclinical studies to determine how BCE works have yielded conflicting results. Part of this is because there is not a universally accepted method to standardize the dose of black cohosh triterpenes, the presumed active ingredients in the extract. Although the mechanism by which BCE relieves symptoms is unknown, several hypotheses have been proposed: it acts 1) as a selective estrogen receptor modulator, 2) through serotonergic pathways, 3) as an antioxidant, or 4) on inflammatory pathways. We found that while the most prominent triterpene in BCE, 23-epi-26-deoxyactein, suppresses cytokine-induced nitric oxide production in brain microglial cells, the whole BCE extract actually enhanced this pathway. A variety of activities have been reported for black cohosh and its compounds, but the absorption and tissue distribution of these compounds is unknown.

No MeSH data available.


Related in: MedlinePlus

NO production from cytokine-induced BV-2 cells pretreated with A) 23-epi-26-deoxyactein (Actein) or B) cimiracemoside-A (CimA). Data are expressed as mean % of cytokine-treated control ± SE. *P < 0.05 vs cytokine control.
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f2-imi-2008-021: NO production from cytokine-induced BV-2 cells pretreated with A) 23-epi-26-deoxyactein (Actein) or B) cimiracemoside-A (CimA). Data are expressed as mean % of cytokine-treated control ± SE. *P < 0.05 vs cytokine control.

Mentions: Typically, unstimulated BV-2 cells produced less than 5 μM NO. BV-2 cells stimulated for 18 hours with IFNγ produced 38 ± 7 μM NO. BV-2 cells stimulated for 18 hours with LPS produced 29 ± 6 μM NO. 30 μg/ml 23-epi-26-deoxyactein had no effect on NO production, but inhibited IFNγ-induced NO production in a dose dependent fashion up to 14%, with a slight increase observed at the lower doses (0.3 μg/ml) of 23-epi-26 deoxyactein (Fig. 2A). 30 μg/ml 23-epi-26-deoxyactein slightly stimulated LPS-induced NO production (Fig. 2A). 13 μg/ml cimiracemoside A slightly decreased NO production after induction by IFNγ (Fig. 2B).


Black Cohosh: Insights into its Mechanism(s) of Action.

Ruhlen RL, Sun GY, Sauter ER - Integr Med Insights (2008)

NO production from cytokine-induced BV-2 cells pretreated with A) 23-epi-26-deoxyactein (Actein) or B) cimiracemoside-A (CimA). Data are expressed as mean % of cytokine-treated control ± SE. *P < 0.05 vs cytokine control.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC3046019&req=5

f2-imi-2008-021: NO production from cytokine-induced BV-2 cells pretreated with A) 23-epi-26-deoxyactein (Actein) or B) cimiracemoside-A (CimA). Data are expressed as mean % of cytokine-treated control ± SE. *P < 0.05 vs cytokine control.
Mentions: Typically, unstimulated BV-2 cells produced less than 5 μM NO. BV-2 cells stimulated for 18 hours with IFNγ produced 38 ± 7 μM NO. BV-2 cells stimulated for 18 hours with LPS produced 29 ± 6 μM NO. 30 μg/ml 23-epi-26-deoxyactein had no effect on NO production, but inhibited IFNγ-induced NO production in a dose dependent fashion up to 14%, with a slight increase observed at the lower doses (0.3 μg/ml) of 23-epi-26 deoxyactein (Fig. 2A). 30 μg/ml 23-epi-26-deoxyactein slightly stimulated LPS-induced NO production (Fig. 2A). 13 μg/ml cimiracemoside A slightly decreased NO production after induction by IFNγ (Fig. 2B).

Bottom Line: Although the mechanism by which BCE relieves symptoms is unknown, several hypotheses have been proposed: it acts 1) as a selective estrogen receptor modulator, 2) through serotonergic pathways, 3) as an antioxidant, or 4) on inflammatory pathways.We found that while the most prominent triterpene in BCE, 23-epi-26-deoxyactein, suppresses cytokine-induced nitric oxide production in brain microglial cells, the whole BCE extract actually enhanced this pathway.A variety of activities have been reported for black cohosh and its compounds, but the absorption and tissue distribution of these compounds is unknown.

View Article: PubMed Central - PubMed

Affiliation: Departments of Surgery and.

ABSTRACT
The Women's Health Initiative found that combination estrogen and progesterone hormone replacement therapy increases breast cancer and cardiovascular disease risk, which compelled many women to seek herbal alternatives such as black cohosh extract (BCE) to relieve their menopausal symptoms. While several clinical trials document the efficacy of BCE in alleviating menopausal symptoms, preclinical studies to determine how BCE works have yielded conflicting results. Part of this is because there is not a universally accepted method to standardize the dose of black cohosh triterpenes, the presumed active ingredients in the extract. Although the mechanism by which BCE relieves symptoms is unknown, several hypotheses have been proposed: it acts 1) as a selective estrogen receptor modulator, 2) through serotonergic pathways, 3) as an antioxidant, or 4) on inflammatory pathways. We found that while the most prominent triterpene in BCE, 23-epi-26-deoxyactein, suppresses cytokine-induced nitric oxide production in brain microglial cells, the whole BCE extract actually enhanced this pathway. A variety of activities have been reported for black cohosh and its compounds, but the absorption and tissue distribution of these compounds is unknown.

No MeSH data available.


Related in: MedlinePlus