مقالات پذیرفته شده در سومین کنگره بین المللی زیست پزشکی
Chrysin suppress breast cancer development
Chrysin suppress breast cancer development
Elham Anari,1,Hamidreza Pazoki-Toroudi,2,*
1. Iran University of Medical Sciences,, Tehran, Iran 2. Dept. of Physiology, Iran University of Medical Sciences,, Tehran, Iran
Introduction: Inflammatory diseases such as neoplasia are believed to cause a leap in Inflammatory leukocytes and chemokines which have been reported as cancer development promoters in many types of cancer such as gastric, intestinal, ovarian, breast and prostate cancer due to their bioactive mediators and plasticity. In the case of Breast cancer, some documents suggest that chronic inflammation stimulates mammary tumor growth throughout specific mechanisms. Several dietary flavones (included kaempferol, quercetin, apigenin, and chrysin) represent the principal anti-microbial and anti-inflammatory impact on human cells. Cyclin D1, a regulatory protein in the cell proliferation cycle, has been detected to be overexpressed in a variety of human cancers as well as in breast tumors and also functions in the cellular inflammatory response. During this research, Chrysin (5,7-dihydroxyflavone)- a natural component found abundantly in honey, propolis, passion fruit flower extract and gum- has loaded in PLGA-PEG in order to increases the solubility and drug tolerance. And this study was aimed to evaluate the effect of Chrysin-loaded PLGA-PEG on Cyclin D1 gene expression as a marker of tumor progression.
Methods: T47D cell line was cultured in RPMI1640 with 10% FBS and was exposed to various concentrations of pure Chrysin and Chrysin-loaded PLGA-PEG (56 and 76 μ M) for 48, and 72 hours. Proton nuclear magnetic resonance (HNMR), Fourier-transform infrared spectroscopy (FT-IR), and scanning electron microscopy (SEM) were used to delineate the Chrysin loading. In vitro cytotoxicity and IC50 of pure and Nano-Chrysin was studied by the MTT assay. The RNA was exploited and cytotoxic effects of Chrysin on Cyclin D1 gene expression were studied by real-time PCR.
Results: Both pure Chrysin and Nano-Chrysin exposure decreased Cyclin D1 gene expression (p<0.001 for both). Cytotoxic effect of Nano-Chrysin was higher than pure Chrysin. The toxic effect of Chrysin was increased with drug dose elevation, demonstrating the dose-dependent association.
Conclusion: The Nano-Chrysin therapy is developed a novel method that could increase cytotoxicity to cancer cells without damaging the normal cells and would be promising in breast cancer therapy.