Melatonin protects MG63 osteoblast-like cells from hydrogen peroxide-induced cytotoxicity by maintaining mitochondrial function.
Melatonin protects MG63 osteoblast-like cells from hydrogen peroxide-induced cytotoxicity by maintaining mitochondrial function.
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DOI：
10.3892/mmr.2013.1832
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发表时间：
2014-02
影响因子：
3.4
通讯作者：
Fei She;Wenbo Wang;Yan Wang;P. Tang;Junqiang Wei;Hua Chen;Bo-xun Zhang
中科院分区：
文献类型：
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作者：
Fei She;Wenbo Wang;Yan Wang;P. Tang;Junqiang Wei;Hua Chen;Bo-xun Zhang
骨质疏松症是一种与活性氧（ROS）诱导的细胞毒性相关的骨骼疾病。线粒体功能障碍可能参与了ROS诱导细胞毒性的潜在机制。已有研究表明，在多种氧化损伤模型中，褪黑素可通过改善线粒体能量代谢和功能发挥细胞保护作用。在本研究中，将MG63成骨样细胞系暴露于不同浓度的过氧化氢（H₂O₂；0、100、200、400或800微摩尔）中8小时，以及暴露于200或400微摩尔的H₂O₂中不同时间段（0.5、4、8或12小时）。结果显示，H₂O₂显著降低了MG63细胞的活力，增加了乳酸脱氢酶的释放，提高了ROS和丙二醛水平，降低了三磷酸腺苷（ATP）浓度，破坏了线粒体膜电位（ΔΨm），并减少了MG63细胞中的线粒体DNA拷贝数。然而，用褪黑素预处理有效地减轻了H₂O₂在MG63细胞中诱导的所有这些细胞毒性和线粒体功能障碍变化。褪黑素的保护作用可能归因于其在H₂O₂处理的细胞中维持线粒体功能的能力。本研究表明，褪黑素是一种潜在的药物，可用于预防如骨质疏松症等疾病中ROS诱导的骨质流失。
Osteoporosis is a bone disease that has been connected with reactive oxygen species (ROS)-induced cytotoxicity. Mitochondrial dysfunction may be involved in the mechanism underlying ROS-induced cytotoxicity. It has been demonstrated that melatonin may exert cytoprotective effects by improving mitochondrial energetics and functions in several models of oxidative damage. In the present study, the MG63 osteoblast-like cell line was exposed to different concentrations of hydrogen peroxide (H2O2; 0, 100, 200, 400 or 800 µM) for 8 h, and 200 or 400 µM H2O2 for various periods of time (0.5, 4, 8 or 12 h). Results showed that H2O2 significantly reduced cell viability, increased the release of lactate dehydrogenase, increased the levels of ROS and malondialdehyde, reduced the concentration of adenosine-5'-triphosphate, disrupted the mitochondrial membrane potential (ΔΨm) and decreased the mitochondrial DNA copy number in MG63 cells. However, pretreatment with melatonin effectively decreased all of these H2O2-induced changes in cytotoxicity and mitochondrial dysfunction in MG63 cells. The protective effects of melatonin may be attributed to its ability to maintain mitochondrial function in H2O2-treated cells. This study suggests that melatonin is a potential pharmacological agent for preventing ROS-induced bone loss in diseases such as osteoporosis.