| Description: |
Actein has a stimulatory effect on osteoblastic bone formation or has potential activity against osteoporosis, it also can prevent oxidative damage to osteoblasts in osteoporotic patients. Actein's ability to pathways involved in lipid disorders and carcinogenesis may make it a new agent for preventing and treating these major disorders, it has been shown to inhibit the proliferation of human breast cancer cells, by altering the activity of the ER IP3 receptor and Na,K-ATPase, inducing calcium release and modulating the NF-κB and MEK pathways. |
| Targets: |
cAMP | TNF-α | NF-kB | Sodium Channel | ATPase | Potassium Channel | MEK | p53 | Akt | P450 (e.g. CYP17) |
| In vitro: |
| J Med Food. 2014 Apr;17(4):414-23. | | Actein isolated from black cohosh promotes the function of osteoblastic MC3T3-E1 cells.[Pubmed: 24552231] | Actein, isolated from black cohosh, was subjected to in vitro experiments to investigate its functional bioactivities in osteoblastic MC3T3-E1 cells.
METHODS AND RESULTS:
Actein caused a significant elevation of alkaline phosphatase activity, collagen synthesis, osteocalcin production, mineralization, and glutathione content in the cells, suggesting that Actein has a stimulatory effect on osteoblastic bone formation or has potential activity against osteoporosis. We investigated the protective effects of Actein on mitochondrial electron transport inhibitor, antimycin A induced toxicity in osteoblastic MC3T3-E1 cells. Exposure of MC3T3-E1 cells to antimycin A caused significant decrease in cell viability and mineralization. However, pretreatment with Actein prior to antimycin A exposure significantly reduced antimycin A-induced cell damage by preventing mitochondrial membrane potential dissipation, complex IV inactivation, cardiolipin oxidation, ROS release, and nitrotyrosine increase, suggesting that Actein may be useful for protecting mitochondria against a burst of oxidative stress. In addition, Actein increased the phosphorylation of CREB (cAMP-response element-binding protein) inhibited by antimycin A and decreased the production of TNF-α induced by antimycin A.
CONCLUSIONS:
These findings suggest that Actein could prevent oxidative damage to osteoblasts in osteoporotic patients. |
|
| In vivo: |
| Fundam Clin Pharmacol. 2009 Jun;23(3):311-21. | | Actein activates stress- and statin-associated responses and is bioavailable in Sprague-Dawley rats.[Pubmed: 19527300] | The purpose of this study was to assess in rats the pharmacological parameters and effects on gene expression in the liver of the triterpene glycoside Actein. Actein, an active component from the herb black cohosh, has been shown to inhibit the proliferation of human breast cancer cells.
METHODS AND RESULTS:
To conduct our assessment, we determined the molecular effects of Actein on livers from Sprague-Dawley rats treated with Actein at 35.7 mg/kg for 6 and 24 h. Chemogenomic analyses indicated that Actein elicited stress and statin-associated responses in the liver; Actein altered expression of cholesterol and fatty acid biosynthetic genes, p53 pathway genes, CCND1 and ID3. Real-time RT-PCR validated that Actein induced three time-dependent patterns of gene expression in the liver: (i) a decrease followed by a significant increase of HMGCS1, HMGCR, HSD17B7, NQO1, S100A9; (ii) a progressive increase of BZRP and CYP7A1 and (iii) a significant increase followed by a decrease of CCND1 and ID3. Consistent with Actein's statin- and stress-associated responses, Actein reduced free fatty acid and cholesterol content in the liver by 0.6-fold at 24 h and inhibited the growth of human HepG2 liver cancer cells. To determine the bioavailability of Actein, we collected serum samples for pharmacokinetic analysis at various times up to 24 h.
The serum level of Actein peaked at 2.4 microg/mL at 6 h.
CONCLUSIONS:
Actein's ability to alter pathways involved in lipid disorders and carcinogenesis may make it a new agent for preventing and treating these major disorders. |
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Cell. 2018 Jan 11;172(1-2):249-261.e12. doi: 10.1016/j.cell.2017.12.019.IF=36.216(2019)
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