Effects of mechanical strain on oxygen free radical system in bone marrow mesenchymal stem cells from children
Effects of mechanical strain on oxygen free radical system in bone marrow mesenchymal stem cells from children
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DOI:
10.1016/j.injury.2010.11.015
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发表时间:
2011-08-01
影响因子:
2.5
通讯作者:
Ni, Guoxin
中科院分区:
文献类型:
--
作者:
Li, Runguang;Chen, Bin;Ni, Guoxin
Background: Physiological loading is widely believed to be beneficial in maintaining skeletal integrity by stimulating new bone formation through increases in osteoblastic activity and concomitant decreases in osteoclastic activity. However, excessive or nonphysiological loading is associated with bone injuries, including stress fractures and osteoporotic fractures, thereby leading to a decreased functional capacity of bone. It is known that the excessive generation of reactive oxygen species (ROS) is a significant factor underlying tissue injury observed in many disease states. The aim of this study was to study the effects of mechanical strain on oxygen free radical system [ROS, superoxide dismutase (SOD) and malondialdehyde (MDA)] in bone marrow mesenchymal stem cells (MSCs) from children.Methods: To determine whether extreme levels of mechanical strain enhance ROS synthesis, we loaded cyclic tensile stretch of varying magnitude on MSCs. After MSCs were stimulated by mechanical strain, ROS labelled with 2,7-dichlorodihydrofluorescein (DCFH) fluorescent probe in cells were detected by flow cytometry (FCM) whilst SOD activity and MDA level were detected by xanthine oxidase method and thiobarbituric acid method, respectively.Results: Extreme levels (>12%) of mechanical strain applied to children's MSCs enhanced ROS synthesis, decreased the activity of SOD and increased the level of MDA, in a time- and magnitude-dependent fashion.Conclusions: These data suggest that excessive magnitude of cyclic tensile strain (> 12%) could induce oxygen free radical disequilibrium, resulting in cytotoxicity. The findings may have clinical implications for orthopaedic practice. (C) 2010 Elsevier Ltd. All rights reserved.