This study was performed to evaluate the antioxidant, anticancer, and toxicity properties of ferutinin, a phytoestrogen derived from Ferula species. The human Michigan Cancer Foundation‐7 (MCF‐7) breast cancer cell line and normal human fibroblast (HDF) were cultured and treated with different ferutinin concentrations. The cell viability was evaluated by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay and cell death‐defining tests (a comparative real‐time polymerase chain reaction [for Bax and Bcl‐2 genes], flow cytometry, and acridine orange/propidium iodide cell staining). Moreover, 15 white male balb/c mice were divided into three groups of five (one untreated control group and two groups), which received different doses of ferutinin‐supplemented water (500 and 1000 µg/kg mice weight) to check the mice liver and kidney pathomorphological alterations and to determine the antioxidant enzymes' expression profile (superoxide dismutase [SOD], catalase [CAT], and glutathione peroxidase) in the mentioned tissues. Finally, the liver lipid peroxidation of mice was analyzed. The results of MTT and cell death‐defining tests indicate the significant reduction in cell viability and induction of apoptotic death in MCF‐7 cells (enhanced sub‐G1 peaks, Bax overexpression, Bcl‐2 downregulation, and increased apoptotic cells). The antioxidant enzymes (SOD and CAT) in the mice liver and kidney cells were found to be upregulated (p < .05) in response to the increasing doses of ferutinin. Besides, the lipid peroxidation of the liver tissue of mice was significantly reduced. According to the results, we suggest that ferutinin has the potential to be served as a selective anticancer compound for breast cancer treatment.

中文翻译：

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Ferutinin：来自阿魏的植物雌激素及其抗癌，抗氧化剂和毒性

进行这项研究是为了评估Ferutinin（一种来自Ferula的植物雌激素）的抗氧化剂，抗癌性和毒性。物种。培养人类密歇根州癌症基金会-7（MCF-7）乳腺癌细胞系和正常人成纤维细胞（HDF），并用不同浓度的Ferutinin对其进行处理。通过3-（4,5-二甲基噻唑-2-基）-2,5-二苯基溴化四氮唑（MTT）分析和确定细胞死亡的试验（比较实时聚合酶链反应[用于Bax和Bcl] ‐2基因]，流式细胞仪和a啶橙/碘化丙啶细胞染色）。此外，将15只白色的雄性balb / c小鼠分为三组，每组五只（一组未治疗的对照组和两组），分别接受不同剂量的补充铁蛋白的水（500和1000 µg / kg小鼠体重）以检查小鼠肝脏和肾脏的病理形态学改变，并确定抗氧化酶的表达特征（超氧化物歧化酶[SOD]，过氧化氢酶[CAT]，和谷胱甘肽过氧化物酶）。最后，对小鼠的肝脂质过氧化进行了分析。MTT和确定细胞死亡的测试结果表明，MCF-7细胞的细胞活力显着降低，并诱导了凋亡的死亡（增强的sub-G1峰，Bax过表达，Bcl-2下调和凋亡细胞增加）。发现小鼠肝脏和肾脏细胞中的抗氧化酶（SOD和CAT）被上调（p  <.05）响应于增加的Ferutinin剂量。此外，小鼠肝脏组织的脂质过氧化作用显着降低。根据结果​​，我们建议阿魏蛋白酶具有用作乳腺癌治疗的选择性抗癌化合物的潜力。