بررسی اثر نانوذره اکسید آهن پوشش دهی شده با گلوکز و کنژوگه شده با سافرانال روی زنده مانی و بیان ژنها در سلولهای رده سرطان کبد.

Autor: سمیه میکائیلی قز, علی صالح زاده, سمیه عطایی جلیسه
Předmět:
Zdroj: Journal of Ilam University of Medical Sciences; 2024, Vol. 32 Issue 5, p50-66, 17p
Abstrakt: Introduction: The high incidence and mortality rates of liver cancer have raised concerns about the effectiveness of current treatments. This study aimed to synthesize iron oxide nanoparticles coated with glucose and conjugated with Safranal (Fe3O4@Glu-Safranal) and investigate its effect on the viability and expression of the CASP8, CASP9, p53, and CAD genes in a liver cancer cell line (HepG2). Materials & Methods: HepG2 cells were treated with different concentrations of the nanoparticles, and the effect of nanoparticles on cell viability was determined using the MTT test. After determining the inhibitory percentage of different concentrations of nanoparticles, the cells were treated with 50% inhibitory concentration of the nanoparticles, their total RNA was extracted, cDNA was synthesized, and gene expression level was evaluated by real-time PCR. The statistical tests included one-way ANOVA and paired t-test, which were analyzed by SPSS V.22 at a level of significance less than 0.05. Results: The results showed that the Fe3O4@Glu-Safranal nanoparticle at concentrations higher than 62.5 µg/ml causes a significant decrease in the survival rate of cancer cells. A 50% inhibitory concentration of the nanoparticle for liver cancer cell lines was found to be 277 and 458 μg/ml, respectively. This showed that the nanoparticle had stronger cytotoxic effects on cancer cells. Also, it was observed that treatment of the cells with Fe3O4@Glu-Safranal caused a significant increase in the expression of the CASP8, CASP9, p53, and CAD genes by 4.27, 2.09, 3.92, and 1.76 folds, respectively, in liver cancer cells (P < 0.05). Conclusion: Apoptosis induction can be considered the main anticancer mechanism of the Fe₃O₄@Glu-Safranal nanoparticle, which is caused in response to direct cell damage or generated oxidative stress. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index