薯蓣皂苷元对人乳腺癌细胞株MCF-7和n -亚硝基-n -甲基脲(NMU)诱导的实验性乳腺癌具有良好的抑制作用

Jayaraman Jagadeesan , Kulanthaivel Langeswaran , Subbaraj Gowthamkumar , Maruthaiveeran Periyaswamy Balasubramanian
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引用次数: 11

摘要

本研究旨在探讨薯蓣皂苷元对人乳腺癌细胞系MCF-7的影响,并探讨其对nmu诱导的实验性乳腺癌的治疗潜力。用不同浓度的薯蓣皂苷元处理乳腺癌细胞,采用MTT法、乳酸脱氢酶渗漏法和谷胱甘肽测定法测定其细胞毒性。n -亚硝基-n -甲基脲(n -nitroso- n - methyllurea, NMU)是一种高度可靠的致癌物质、诱变剂和致畸剂,在本研究中用于促进实验大鼠乳腺癌的发生。在体外研究中,薯蓣皂苷元以剂量依赖的方式显著抑制MCF-7细胞的增殖,并且由于药物的细胞毒性,在MCF-7细胞中观察到GSH的消耗和LDH活性的增加。nmu诱导的乳腺癌动物脂质过氧化水平升高被降低(P <0.05),这是由于甾体薯蓣皂苷元的管理。改变的溶酶体酶被薯蓣皂苷元中和,并且由于其抗氧化活性,它可以保护大分子损伤免受氧化应激和游离自由基的产生。本研究结果提示薯蓣皂苷元可能作为一种化学保护剂用于人乳腺癌的治疗。
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Diosgenin exhibits beneficial efficiency on human mammary carcinoma cell line MCF-7 and against N-nitroso-N-methylurea (NMU) induced experimental mammary carcinoma

The purpose of the present study was to investigate the impact of diosgenin on the human mammary carcinoma cell line (MCF-7) and to investigate its therapeutic potential against NMU-induced experimental breast cancer. Mammary carcinoma cells were treated with different concentrations of diosgenin and its cytotoxicity effect was measured by MTT method, lactate dehydrogenase leakage and by estimating GSH assays. N-nitroso-N-methylurea (NMU) is a highly reliable carcinogen, mutagen and teratogen used in the present study to promote breast carcinogenesis in experimental rats. In in vitro studies, diosgenin significantly inhibited the proliferation of MCF-7 cells in a dose-dependent manner and the depletion of GSH and an increase of LDH activity were observed in MCF-7 cells due to cytotoxic nature of the drug. Elevated lipid peroxidation in NMU-induced breast cancer-bearing animals were drim down (P < 0.05) due to management with steroidal diosgenin. The altered lysosomal enzymes were neutralised by diosgenin and also, it protects macromolecular damage from oxidative stress and free fadicals production due to its antioxidant activity. From the results of our present analysis, it gives an idea about that diosgenin may be used as a chemoprotective agent against human mammary carcinoma.

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