Phytotherapy Research · 2010 · 18 citations · 20 references
MedicinePharmacologyToxicologyCarcinogenesisMetabolismMolecular ToxicologyCarcinogen MetabolismCarcinogenicity AssessmentCarcinogenicity Of Dietary ExposuresCellular ToxicologyChemical CarcinogenesisMolecular Mechanisms Of ToxicityArachidonic Acid MetabolitesArachidonic Acid PeroxidationBioactive Plant CompoundsChemical Carcinogen ExposureCyclooxygenase IsoformsMechanisms Of CarcinogenicityPlant-derived CarcinogensProstaglandin Synthesis Inhibition
The main bioactive compounds of Trigonella foenum graecum L. (fenugreek) seeds are protodioscin, trigoneoside, diosgenin and yamogenin, which have anticarcinogenic potency through inhibition of cell proliferation and inhibition of prostaglandin synthesis. The effect of fenugreek on ALOX and COX genes was examined in AKR/J H-2(k) mice exposed to dimethylbenz[α]anthracene (DMBA), a potent carcinogen. The expression pattern of these genes was determined by detecting the mRNA expression in various tissues (the lungs, liver, spleen and the kidneys) in four groups of mice. Two groups were fed with normal and two of them with fenugreek containing nutriment. Each group divided into DMBA treated and control groups. Mice were autopsied on day 7 after DMBA treatment for mRNA isolation. Fenugreek consumption itself did not change gene expression compared with the control group. DMBA could increase the expression of ALOX12, ALOX15, ALOX5 genes mainly in all organs. Fenugreek consumption was generally protective in each organ in a different manner. DMBA treatment increased COX2 gene expression, but fenugreek was protective in all tissues examined. In COX1 gene, the fenugreek diet could suppress the expression, except for spleen, independently from carcinogen exposure. Therefore by inhibiting the arachidonic acid metabolism fenugreek may prevent tumorigenesis.
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