Expression of heme oxygenase-1 due to intracellular reactive oxygen species induced by ultrasound
Expression of heme oxygenase-1 due to intracellular reactive oxygen species induced by ultrasound
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DOI：
10.1016/j.ultsonch.2005.09.004
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发表时间：
2006-07-01
影响因子：
8.4
通讯作者：
Kondo, Takashi
中科院分区：
文献类型：
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作者：
Kagiya, Go;Ogawa, Ryohei;Kondo, Takashi
本研究旨在阐明超声诱导血红素氧合酶-1（HO-1）表达的机制。当人淋巴瘤U937细胞暴露于1 MHz的连续波1分钟，HO-1的表达通过实时定量聚合酶链反应和免疫印迹检测，观察强度以上的空化阈值。没有观察到HO-1表达的诱导在暴露于42摄氏度的温度比在超声处理过程中的温度高1分钟的细胞。当一个有效的抗氧化剂，N-乙酰-L-半胱氨酸，加入到培养基之前或之后的超声处理，诱导减弱，表明活性氧（ROS）参与。然而，添加过氧化氢酶并不影响诱导，并且在添加预超声处理的培养基时没有观察到HO-1，这表明由于细胞外产生的羟基自由基的重组而导致的过氧化氢不参与。自由基清除剂谷胱甘肽单乙酯、二甲基亚砜和D（-）-甘露醇的加入抑制了诱导。线粒体膜电位的下降和超氧化物的产生也观察到在超声处理的细胞，这表明线粒体是细胞内产生的ROS的来源。这些结果表明，超氧化物从受损的线粒体，而不是在培养基中直接产生的羟基自由基，产生细胞内的氧化应激诱导HO-1的表达。(c)2005 Elsevier B. V.保留所有权利。
The present study was undertaken to elucidate the mechanism by which ultrasound induces the expression of heme oxygenase-1 (HO-1). When human lymphoma U937 cells were exposed to a 1 MHz continuous wave for I min, HO-1 expression examined by real-time quantitative polymerase chain reaction and immunoblotting was observed at intensities above the cavitational threshold. No induction of HO-1 expression was observed in the cells exposed for I min to 42 degrees C a temperature higher than that during sonication. When a potent antioxidant, N-acetyl-L-cysteine, was added to the culture medium before or after sonication, the induction was attenuated, indicating that reactive oxygen species (ROS) are involved. However, the addition of catalase did not affect the induction, and no HO-1 was observed on the addition of pre-sonicated medium, suggesting that hydrogen peroxide due to the recombination of hydroxyl radicals generated extracellularly was not involved. The addition of free radical scavengers, glutathion-monoethyl ester, dimethyl sulfoxide and D(-)-mannitol, suppressed the induction. A decrease in mitochondrial membrane potential and the generation of superoxide were also observed in the sonicated cells, suggesting that mitochondria were the source of intracellularly generated ROS. These results indicate that superoxide secondarily generated from damaged mitochondria, not hydroxyl radicals generated in medium directly by sonication, give rise to intracellular oxidative stress inducing HO-1 expression. (c) 2005 Elsevier B.V. All rights reserved.