Department of Orthopaedic Surgery, Yijishan Hospital, Wannan Medical College, Wuhu, Anhui, China.
Orthop Surg. 2009 May;1(2):144-52. doi: 10.1111/j.1757-7861.2009.00019.x.
Curcumin, an active ingredient derived from the rhizome of the plant, Curcuma longa, has antioxidant, anti-inflammatory and anti-cancer activities. The aims of this study were to examine whether curcumin can induce apoptosis in an osteosarcoma cell line.
Curcumin-induced apoptosis in human osteosarcoma U2OS cells was investigated using morphological analysis, marked nuclear condensation and fragmentation of chromatin, which were observed by Hoechst 33258 staining and DNA ladder formation. The U2OS cells were treated with or without curcumin. Cell viability was assessed by the 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium (MTT) method. Cell-cycle, apoptosis and apoptosis-related proteins in U2OS cells were evaluated by flow cytometry and western blotting.
Curcumin showed growth inhibitory effects on U2OS cells in a dose-and time-dependent manner, inducing significant G1 arrest and apoptosis in U2OS cells. This curcumin-induced apoptosis in U2OS cells was accompanied by up-regulation of Bax, Bak, and p-Bad and down-regulation of Bcl-2, but no effect on the levels of Bcl-X(L) or Bad proteins was noted. Moreover, curcumin treatment resulted in a significant reduction of mitochondrial membrane potential and increase in the concentrations of mitochondrial cytochrome C and caspase-3.
Multiple molecular pathways are involved in curcumin-induced apoptosis of human U2OS cells. These include pro-and anti-apoptotic Bcl-2 family proteins, mitochondrial membrane potential, mitochondrial cytochrome C and caspase-3.
姜黄素是从植物姜黄的根茎中提取的一种有效成分,具有抗氧化、抗炎和抗癌作用。本研究旨在探讨姜黄素是否能诱导骨肉瘤细胞系发生细胞凋亡。
采用 Hoechst 33258 染色和 DNA 梯状带形成观察核染色质固缩和碎裂的形态学分析,研究姜黄素对人骨肉瘤 U2OS 细胞凋亡的诱导作用。用或不用姜黄素处理 U2OS 细胞。通过 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑(MTT)法评估细胞活力。用流式细胞术和 Western blot 法评估 U2OS 细胞的细胞周期、凋亡和凋亡相关蛋白。
姜黄素呈剂量和时间依赖性抑制 U2OS 细胞生长,诱导 U2OS 细胞明显的 G1 期阻滞和凋亡。这种姜黄素诱导的 U2OS 细胞凋亡伴随着 Bax、Bak 和 p-Bad 的上调以及 Bcl-2 的下调,但 Bcl-X(L)或 Bad 蛋白水平没有变化。此外,姜黄素处理导致线粒体膜电位显著降低,线粒体细胞色素 C 和 caspase-3 浓度增加。
多种分子途径参与了姜黄素诱导的人 U2OS 细胞凋亡。这些途径包括促凋亡和抗凋亡的 Bcl-2 家族蛋白、线粒体膜电位、线粒体细胞色素 C 和 caspase-3。