Natural Products from Cimicifuga foetida

Cimitriteromone A-G, Macromolecular Triterpenoid-Chromone Hybrids from the Rhizomes of Cimicifuga foetida.[Pubmed: 30044102]

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Influence of hormone therapy or C. foetida extract on breast tenderness in postmenopausal women.[Pubmed: 29542344]

To evaluate the prevalence of breast tenderness in a population treated with menopausal hormone therapy (MHT) or Cimicifuga foetida extract.

Efficacy and safety evaluation of Cimicifuga foetida extract in menopausal women.[Pubmed: 29198157]

The aim of this study was to evaluate the efficacy and safety of long-term treatment with Cimicifuga foetida extract in menopausal women.

Actein ameliorates hepatic steatosis and fibrosis in high fat diet-induced NAFLD by regulation of insulin and leptin resistant.[Pubmed: 29156528]

Insulin and leptin resistance are highly involved in metabolic syndrome and non-alcoholic fatty liver disease (NAFLD). Presently, no approved treatment is available. Actein is isolated from the rthizomes of Cimicifuga foetida, a triterpene glycoside, exhibiting important biological properties, such as anti-inflammatory, anti-cancer, and anti-oxidant activity. However, its effects on metabolic syndrome are poorly understood. The aims of the study were mainly to investigate the molecular mechanisms regulating insulin and leptin resistance, and lipogenic action of actein in high fat diet-fed mice. Our data indicated that actein-treated mice displayed lower body weight, epididymal and subcutaneous fat mass, as well as serum lipid levels. Also, improved insulin and leptin resistance were observed in actein-treated groups. Liver inflammation and fibrosis triggered by high fat diet were decreased for actein administration. Moreover, hepatic lipid accumulation was also reduced by actein along with reductions of hepatic de novo lipogenesis-linked signals in actein-treated rodents with high fat diet. High fat diet-induced activation of insulin receptor substrate 1/Forkhead box protein O1 (IRS1/FOXO1), Janus kinase 2 gene/signal transducer and activator of transcription (JAK2/STAT3) and Protein Kinase B/Glycogen synthase kinase 3 beta (AKT/GSK3β) pathways in liver was inhibited by actein, a potential mechanism by which hyperinsulinemia, hyperleptindemia and dyslipidemia were attenuated. Thus, the findings above might be of nutritional and therapeutic importance for the treatment of NAFLD.

Actein induces apoptosis in leukemia cells through suppressing RhoA/ROCK1 signaling pathway.[Pubmed: 29039493]

Actein is a tetracyclic triterpenoid compound, extracted from the rhizome of Cimicifuga foetida, exhibiting anticancer activities as previously reported. However, the effects of actein on human leukemia have not been explored before. In this study, the role of actein in regulating apoptosis induction in human leukemia cells was investigated. Actein administration significantly enhanced apoptosis, especially in human leukemia cell line of U937 and the primary human leukemia cells. The promotion was accompanied by caspase-9, caspase-3 and poly(ADP-ribose) polymerase (PARP) cleavage, and cytochrome c (Cyto-c) release. Additionally, translocation of Bax into mitochondria was increased by actein, while anti-apoptotic signals of myeloid cell leukemia-1 (Mcl-1) and B cell CLL/lymphoma 2 (Bcl-2) were decreased, accompanied by reduced phosphorylated Bcl-2-associated death promoter (Bad). Furthermore, protein kinase B (AKT) activation was downregulated by actein treatment in U937 cells. RhoA, but not caspase-3, regulated Rho kinase 1 (ROCK1) expression induced by actein. Suppression of RhoA and ROCK1 reduced ROCK1 expression, caspase-9, caspase-3 and PARP cleavage. In contrast, AKT inactivity enhanced apoptosis levels, as well as caspase signaling pathway expression. The anticancer role of actein was potentiated by inactivating AKT. In vivo, U937-bearing tumor growth was suppressed by actein, which was related to ROCK1 suppression, AKT dephosphorylation and apoptosis induction. These results indicated that actein has a suppressive role in human leukemia progression through inactivating RhoA/ROCK1 and inducing caspases.

Cimicifoetones A and B, Dimeric Prenylindole Alkaloids as Black Pigments of Cimicifuga foetida.[Pubmed: 28393490]

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