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Apigenin

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(CAS#: 520-36-5)

 

Apigenin is a flavone that is the aglycone of apiin, isolated from parsley and celery, and apigetrin. It is a yellow crystalline solid that has been used to dye wool.

Synonyms: 5,7,4'-trihydroxyflavone

Molecular Formula: C15H10O5

Brief:

Foods rich in apigenin include apples, endive, beans, broccoli, celery, cherries, cloves, grapes, leeks, onions, barley, parsley and tomatoes, while plant-derived beverages containing apigenin include tea and wine. Apigenin is natural flavonoid present in the leaves and stems of vascular plants, including fruits and vegetables.

Pharmacology:

Anticarcinogenic Activity.Antiviral agents for the treatment of HIV and other infections£¬inhibitor of MAP kinase£¬treatment of diseases including inflammatory bowel disease and skin conditions¡£Antioxidant and Pro-oxidant Effects.

Advanced Research:

Apigenin significantly induced glutathione transferase (GST) in Wistar rat heart, suggesting that it might function as a specific protectant against cardiotoxic agents.Anti-spasmodic in Parkinson's disease.

Articles:

1. Pharmacological profile of apigenin, a flavonoid isolated from Matricaria chamomilla.

Dried flowers of Matricaria chamomilla L. are largely used to provide sedative as well as spasmolytic effects. In the present study, we examined in particular the pharmacological property of a fraction isolated from a methanolic extract of M. chamomilla, which was identified by HPLC-MS-MS analysis as apigenin. By radioreceptor binding assays, we demonstrated the ability of the flavone to displace a specific radioligand, [(3)H]Ro 15-1788, from the central benzodiazepine binding site. Electrophysiological studies performed on cultured cerebellar granule cells showed that apigenin reduced GABA (gamma-aminobutyric acid)-activated Cl(-) currents in a dose-dependent fashion. The effect was blocked by co-application of Ro 15-1788, a specific benzodiazepine receptor antagonist. Accordingly, apigenin reduced the latency in the onset of picrotoxin-induced convulsions. Moreover, apigenin injected i.p. in rats reduced locomotor activity, but did not demonstrate anxiolytic, myorelaxant, or anticonvulsant activities. The present results seem to suggest that the inhibitory activity of apigenin on locomotor behaviour in rats cannot be ascribed to an interaction with GABA(A)-benzodiazepine receptor but to other neurotransmission systems, since it is not blocked by Ro 15-1788.

2.Molecular targets for apigenin-induced cell cycle arrest and apoptosis in prostate cancer cell xenograft

Apigenin (4',5,7-trihydroxyflavone) is a promising chemopreventive agent abundantly present in fruits and vegetables that has been shown to promote cell cycle arrest and apoptosis in various malignant cell lines. To determine whether pharmacologic intervention with apigenin has a direct growth inhibitory effect on human prostate tumors implanted in athymic nude mice, we examined cell cycle regulatory molecules as precise molecular targets of apigenin action. Apigenin feeding by gavage to these mice at doses of 20 and 50 ¦Ìg/mouse/d in 0.2 mL of a vehicle containing 0.5% methyl cellulose and 0.025% Tween 20 resulted in significant decreases in tumor volume and mass of androgen-sensitive 22Rv1 and androgen-insensitive PC-3-implanted cells. Oral intake of apigenin resulted in dose-dependent ( a ) increase in the protein expression of WAF1/p21, KIP1/p27, INK4a/p16, and INK4c/p18; ( b ) down-modulation of the protein expression of cyclins D1, D2, and E; and cyclin-dependent kinases (cdk), cdk2, cdk4, and cdk6; ( c ) decrease in retinoblastoma phosphorylation at serine 780; ( d ) increase in the binding of cyclin D1 toward WAF1/p21 and KIP1/p27; and ( e ) decrease in the binding of cyclin E toward cdk2 in both types of tumors. In addition, apigenin feeding resulted in stabilization of p53 by phosphorylation at serine 15 in 22Rv1 tumors, which seems to exhibit p53-dependent growth inhibitory responses. Apigenin intake by these mice also resulted in induction of apoptosis, which positively correlated with serum and tumor apigenin levels. Taken together, this is the first systematic in vivo study showing the involvement of cell cycle regulatory proteins as potential molecular targets of apigenin. [Mol Cancer Ther 2006;5(4):843¨C52]