Apoptosis induced by the sonornechanical effects of low intensity pulsed ultrasound in a human leukemia cell line
Apoptosis induced by the sonornechanical effects of low intensity pulsed ultrasound in a human leukemia cell line
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DOI：
10.1016/j.canlet.2004.08.034
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发表时间：
2005-04-28
期刊：
影响因子：
9.7
通讯作者：
Umemura, S
中科院分区：
文献类型：
--
作者：
Feril, LB;Kondo, T;Umemura, S
为了获得一个最佳的条件，超声（US）诱导的细胞凋亡，可能是有用的癌症治疗，我们应用低强度脉冲超声超声在体外超声处理U937细胞。然后在测量细胞凋亡之前以不同的时间间隔孵育细胞。通过DNA片段化和磷脂酰丝氨酸外化来评估细胞凋亡。通过流式细胞术测定线粒体膜电位降低的模式。在超声处理后12小时，1 MHz超声（0.3 W/cm 2，10%占空因数，100 Hz，1 min）达到最佳凋亡（70.0 +/- 13.8%）和2次最小裂解。缺乏US诱导的自由基检测和缺乏血红素加氧酶-1（细胞内氧化应激标志物）在细胞中上调，表明声力学效应而非声化学效应是主要机制。(c)2004爱思唯尔爱尔兰有限公司保留所有权利。
To obtain an optimal condition for ultrasound (US)-induced apoptosis that could be useful for cancer therapy, we applied low intensity pulsed US to sonicate U937 cells in vitro. Cells were then incubated at different time intervals before measuring apoptosis. The apoptosis was assessed by DNA fragmentation and phosphatidylserine externalization. The pattern of the decrease in mitochondrial membrane potential was determined by flow cytometry. Optimal apoptosis (70.0 +/- 13.8%) with 2 minimal lysis was attained with 1 MHz ultrasound 0.3 W/cm(2), 10% duty factor at 100 Hz for 1 min) at 12 h after sonication. Lack of US-induced free radical detection and absence of Heme oxygenase-1, an intracellular oxidative stress marker, up-regulation in cells, suggest that sonomechanical, not sonochemical, effects are the main mechanism involved. (c) 2004 Elsevier Ireland Ltd. All rights reserved.