Hou De-Xing, Tong Xuhui, Terahara Norihiko, Luo Dong, Fujii Makoto
Department of Biochemical Science and Technology, Faculty of Agriculture, Kagoshima University, Korimoto 1-21-24, Kagoshima 890-0065, Japan.
Arch Biochem Biophys. 2005 Aug 1;440(1):101-9. doi: 10.1016/j.abb.2005.06.002.
Delphinidin 3-sambubioside (Dp3-Sam), a Hibiscus anthocyanin, was isolated from the dried calices of Hibiscus sabdariffa L. Dp3-Sam could induce a dose-dependent apoptosis in human leukemia cells (HL-60) as characterized by cell morphology, DNA fragmentation, activation of caspase-3, -8, and -9, and inactivation of poly(ADP)ribose polymerase (PARP). Molecular data showed that Dp3-Sam induced Bid truncation, mitochondrial membrane potential (DeltaPsi(m)) loss, and cytochrome c release from mitochondria to cytosol. Moreover, Dp3-Sam caused a time- and dose-dependent elevation of intracellular reactive oxygen species (ROS) level in HL-60 cells, and antioxidants such as N-acetyl-L-cysteine (NAC) and catalase could effectively block Dp3-Sam-induced ROS generation, caspase-3 activity, and DNA fragmentation. These data indicate that Dp3-Sam might induce apoptosis in HL-60 cells through a ROS-mediated mitochondrial dysfunction pathway. These findings enhance our understanding for anticancer function of Hibiscus anthocyanins in herbal medicine.
矢车菊素3 - 接骨木二糖苷(Dp3 - Sam)是一种木槿属花青素,从玫瑰茄干燥花萼中分离得到。Dp3 - Sam可诱导人白血病细胞(HL - 60)发生剂量依赖性凋亡,其特征表现为细胞形态变化、DNA片段化、半胱天冬酶 - 3、 - 8和 - 9的激活以及聚(ADP)核糖聚合酶(PARP)的失活。分子数据表明,Dp3 - Sam诱导Bid截短、线粒体膜电位(ΔΨm)丧失以及细胞色素c从线粒体释放到细胞质中。此外,Dp3 - Sam导致HL - 60细胞内活性氧(ROS)水平呈时间和剂量依赖性升高,抗氧化剂如N - 乙酰 - L - 半胱氨酸(NAC)和过氧化氢酶可有效阻断Dp3 - Sam诱导的ROS生成、半胱天冬酶 - 3活性及DNA片段化。这些数据表明,Dp3 - Sam可能通过ROS介导的线粒体功能障碍途径诱导HL - 60细胞凋亡。这些发现加深了我们对草药中木槿属花青素抗癌功能的理解。