Anticancer Effect of Amygdalin (Vitamin B-17) on Hepatocellular Carcinoma Cell Line (HepG2) in the Presence and Absence of Zinc

(E-pub Ahead of Print)

Author(s): Mohamed A. El-Desouky, Abdelgawad A. Fahmi*, Ibrahim Y. Abdelkader, Karima M. Nasraldin.

Journal Name: Anti-Cancer Agents in Medicinal Chemistry
(Formerly Current Medicinal Chemistry - Anti-Cancer Agents)

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Abstract:

Background: Amygdalin (Vitamin B-17) is a naturally occurring vitamin found in the seeds of the fruits of Prunus Rosacea family including apricot, bitter almond, cherry, and peach.

Objective: The purpose of this study was to examine the effect of amygdalin with and without zinc on hepatocellular carcinoma (HepG2) cell line.

Methods: MTT assay was used to evaluate the cytotoxicity of amygdalin without zinc, amygdalin + 20µmol zinc, and amygdalin + 800µmol zinc on HepG2 cell lines. The cell cycle distribution assay was determined by flow cytometry. Apoptosis was confirmed by Annexin V-FITC/PI staining assay. Moreover, the pathway of apoptosis was determined by the percentage of change in the mean levels of P53, Bcl2, Bax, cytochrome c, and caspase-3.

Results: Amygdalin without zinc showed a strong anti-HepG2 activity. Furthermore, HepG2 cell lines treatment with amygdalin + 20µmol zinc and amygdalin + 800µmol zinc showed a highly significant apoptotic effect than the effect of amygdalin without zinc. Amygdalin treatment induced the cell cycle arrest at G2/M and increased the levels of P53, Bax, cytochrome c, and caspase-3 significantly, while it decreased the level of anti-apoptotic Bcl2.

Conclusion: Amygdalin is a natural anti-cancer agent which can be used for the treatment of hepatocellular carcinoma. It promotes apoptosis via the intrinsic cell death pathway (the mitochondria-initiated pathway) and cell cycle arrest at G/M. The potency of amygdalin in HepG2 treatment increased significantly by the addition of zinc.

Keywords: Amygdalin, vitamin B-17, hepatocellular carcinoma, anti-cancer, Bcl2, caspase-3, P53, zinc

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(E-pub Ahead of Print)
DOI: 10.2174/1871520620666200120095525
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