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首页> 外文期刊>Drug research >Capillarisin Exhibits Anticancer Effects by Inducing Apoptosis, Cell Cycle Arrest and Mitochondrial Membrane Potential Loss in Osteosarcoma Cancer Cells (HOS)
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Capillarisin Exhibits Anticancer Effects by Inducing Apoptosis, Cell Cycle Arrest and Mitochondrial Membrane Potential Loss in Osteosarcoma Cancer Cells (HOS)

机译:毛细血管素通过诱导骨肉瘤癌细胞(HOS)的凋亡,细胞周期阻滞和线粒体膜电位丧失,表现出抗癌作用。

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The aim of the present study was to assess the anticancer activity of capillarisin against human osteosarcoma (HOS) cancer cells in vitro. Cell viability after capillarisin drug treatment and evaluated by MTT assay. The extent of cell death induced by capillarisin was estimated by using lactate dehydrogenase (LDH) assay. The effect of capillarisin on cell cycle phase distribution and mitochondrial membrane potential (ΛΨm) was demonstrated via flow cytometry using propid-ium iodide (PI) and rhodamine-123 (Rh-123) DNA-binding fluorescent dyes respectively. Fluorescence microscopy was employed to examine the morphological changes in osteosarcoma cancer cells and presence of apoptotic bodies following capillarisin treatment. The results of thisstudy revealed that capillarisin induced dose-dependent growth inhibition of these cancer cells after 12-h of incubation. Further, capillarisin induced significant release of LDH from these cell cultures and this LDH release was much more noticeable at higher concentrations of capillarisin. Hoechst 33258 staining revealed characteristic morphological features of apoptosis triggered by capillarisin treatment. Cell cycle analysis revealed that capillarisin induced dose-dependent G0/G1-phase cell cycle arrest. Capillarisin also trigerred a progressive and dose-dependent reduction in the mitochondrial membrane potential. In conclusion, capillarisin inhibits cancer cell growth of osteosarcoma cells by inducing apoptosis accompanied with G0/G1-phase cell cycle arrest and loss in mitochondrial membrane potential.
机译:本研究的目的是评估毛细管菌素在体外对人骨肉瘤(HOS)癌细胞的抗癌活性。毛细血管毒素药物治疗后的细胞生存力,并通过MTT分析评估。通过使用乳酸脱氢酶(LDH)测定法估计了毛细血管生成素诱导的细胞死亡程度。通过分别使用碘化丙锭(PI)和若丹明-123(Rh-123)DNA结合荧光染料的流式细胞术证明了毛细血管素对细胞周期相分布和线粒体膜电位(Ψm)的影响。荧光显微镜用于检查毛细血管毒素治疗后骨肉瘤癌细胞的形态变化和凋亡小体的存在。这项研究的结果表明,在培养12小时后,毛细血管生成素诱导了这些癌细胞的剂量依赖性生长抑制。此外,毛细血管毒素诱导了这些细胞培养物中LDH的显着释放,并且在更高浓度的毛细血管毒素中,这种LDH释放更为明显。 Hoechst 33258染色显示毛细血管素处理触发的凋亡特征形态学特征。细胞周期分析表明,毛细血管生成素诱导了剂量依赖性的G0 / G1期细胞周期停滞。毛细血管素还触发了线粒体膜电位的逐步和剂量依赖性降低。总之,毛细血管生成素通过诱导凋亡并伴随G0 / G1期细胞周期停滞和线粒体膜电位丧失来抑制骨肉瘤细胞的癌细胞生长。

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