[Latin Name] Cinnamomun camphcra

[Plant Source] It is extracted from Ginkgo Biloba Leaf.

[Specifications]

1, Ginkgo Biloba Extract 24/6

Total Ginkgo flavone glycosides 24%

Total terpene lactones 6%

2, Ginkgo Biloba Extract 24/6

Total Ginkgo flavone glycosides 24%

Total terpene lactones 6%

Ginkgolic acid 5ppm

3,CP2005

Total Ginkgo flavone glycosides 24%

Quercatin: kaemperol 0.8–1.5

Total terpene lactones 6%

Ginkgolic acid <5ppm

4.Germany Standard

Total Ginkgo Flavone Glycosides 22.0%-27%

Total Terpene Lactones 5.0%-7.0%

Bilobalides 2.6%-3.2%

Ginkgolic acid <1ppm

5.Water-Soluble Ginkgo Biloba Extract 24/6

Water Solubility: 5g Ginkgo Biloba Extract will be dissolved completely in 100g water

Total Ginkgo Flavone Glycosides 24.0%

Total Terpene Lactones 6.0%

Ginkgolic acid <5.0ppm

[Appearance] Light yellow fine powder

[Particle size] 80 Mesh

[Loss on drying] £ 5.0%

[Heavy Metal] £10PPM

[Extract solvents] Ethanol

[Storage] Store in cool & dry area, keep away from the direct light and heat.

[Package] Packed in paper-drums and two plastic-bags inside.

[Function]

Expanding blood vessel, resisting insufficient blood and oxygen deficit, increasing blood flow, improving cerebral arteries and distal

blood flow. Promoting cerebral circulation metabolism, improving memory function, resisting depression, resisting lipidic overoxidation,

protecting liver damage.

In clinic, curing high blood pressure, hyperlipoidemia, coronary heart disease, angina pectoris, arterial sclerosis, cerebral embolism,

senile dementia, primary and periodic dropsy, acute drumming in the ears, epicophosis, a variety of body function in disorder, dizziness

and so on.

Recorded on January 23, 2011 using a Flip Video camcorder.

Mechanisms underlying the anti-tumoral effect of Allium roseum L. extract on Chronic Myeloid Leukemia K562 cells

Communication de Soumaya Souid, doctorante à l”IPT, Colloque Jeunes Chercheurs de l’IPT (8-9 décembre 2016)

Background and objectives: Among various strategies that have been explored to overcome tumor drug
resistance, the combination of current chemotherapy with plant extracts as chemosensitizers has emerged
as a promising one. In the present study, we investigated for the first time the anti-cancer activity of Allium
roseum L. extract, a wild edible species in North Africa and its mechanisms against the well-characterized
human Chronic Myelogenous Leukemia (CML) K562 cells in vitro.
Methodology: K562 cells were treated with dehydrated aqueous (DAE) and fresh extracts in a time- and
dose-dependent manner. Cell viability and cytotoxicity were evaluated by MTT and LDH assays. Cell cycle
analysis and the apoptosis levels were assessed by flow cytometry. Using Western blot and Elisa assays, we
elicited key signaling pathways and effectors proteins targeted by DAE.
Results: DAE exhibited the highest antiproliferative activity on K562 cells even compared with the
chemotherapeutic drug Imatinib Mesylate, a tyrosine kinase inhibitor that targets the fusion oncoprotein
BCR-ABL responsible for this disease. DAE disturbed the cell cycle progression and induced the apoptosis
of K562 cells. Chemical analysis of DAE showed a diversity of organosulfur compounds RCSO and high
amount of allicin, suggesting that such molecule may be behind the anti-cancer effect of Allium roseum
extract. Similarly to Imatinib Mesylate, DAE inhibitory effect was associated with the dephosphorylation
of BCR-ABL kinase and interfered with the major prosurvival pathways, ERK1/2 and Akt. Furthermore, we
found that DAE-induced inactivation of Akt kinase led to the activation of its target FOXO3 transcription
factor, enhancing the expression of FOXO3-regulated pro-apoptotic effectors, Bim and Bax, and cell cycle
inhibitor p27. Finally, we found that DAE-treated K562 cells presented a reduced secretion of the proangiogenic
effector, Vascular Endothelial Growth Factor ( VEGF), compared to the non-treated cells.
Conclusion: Our data suggest that Allium roseum L. extract has great potential as a non-toxic cheap and
effective alternative to conventional chemotherapy that presents a dual inhibitory effect on both cancer
cell viability, through FOXO3 activation, and its angiogenic promoting regulator VEGF.