الفهرس | Only 14 pages are availabe for public view |
Abstract Garlic is a vegetable (Allium sativum) that belongs to the Allium class of bulb-shaped plants, which also includes onions, chives, leeks, and scallions. Garlic is used for flavoring in cooking and is unique because of its high sulfur content. Garlic also contains arginine, oligosaccharides, flavonoids, and selenium all of which may be beneficial to health. Garlic has a variety of Benefits effects, as it helps to control: Blood sugar, high cholesterol, chemo-preventive effects, anti-fungal, antibacterial and anti-parasites. Garlic has a variety of anticancer effects including: cancer cell growth inhibition, inhibit the development of chemically induced cancers, block covalent binding of carcinogens to DNA, enhance degradation of carcinogens, have anti-oxidative and free radical scavenging properties, and regulate cell proliferation, apoptosis, and immune responses. In our study, we investigate the anti-cancer effect of garlic extract and its different fractions (as little is known about garlic fractions effect on cancer); petroleum ether, methylene chloride, ethyl acetate and n-butanol on different types of human cell lines as liver cancer cell (HepG2) and Breast cancer cell (MCF-7), determine the change in molecular mechanisms and cell cycle and analysis the best effective garlic fraction which inhibit about 50% of cell with low concentration. Different garlic fractions, extracted by petroleum ether (PE), methylene chloride (MC), ethyl acetate (EtOAc) and n-butanol (B) solvents, each fraction exhibited significant dose-dependent anti-proliferative activity on MCF7 and HepG2 cells with best results for EtOAc with IC50 values 21.32 and 26.22 μg/ml, respectively, as compared to vehicle-treated cells. HPLC analysis revealed the presence of 14 components in EtOAc fraction with highest concentrations for linoleic acid (LA) and S-allylthiocysteine. EtOAc fraction inhibited cancer cells proliferation through induction of apoptosis (revealed by a significant increase in mRNA levels of apoptotic markers, Caspase 3 and Bax and a significant decrease in mRNA levels of the anti-apoptotic marker, Bcl2) and cell cycle arrest in G2/M phase (indicated by increase in number of MCF7 and HepG2 cells in this phase). |