Social disruption stress increases IL-6 levels and accelerates atherosclerosis in ApoE-/- mice
Social disruption stress increases IL-6 levels and accelerates atherosclerosis in ApoE-/- mice
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DOI：
10.1016/j.atherosclerosis.2011.11.041
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发表时间：
2012-04-01
期刊：
影响因子：
5.3
通讯作者：
Bergstrom, Goran M. L.
中科院分区：
文献类型：
--
作者：
Bernberg, Evelina;Ulleryd, Marcus A.;Bergstrom, Goran M. L.
前言：我们先前已经证明，不同形式的应激对小鼠动脉粥样硬化的形成有不同的影响。我们发现，社会压力会增加载脂蛋白E(-/-)小鼠的动脉粥样硬化，而更多的身体形式的压力不会。在这里，我们评估了社会破坏(SDR)应激对动脉粥样硬化形成的影响，并评估了SDR应激和另外5次物理应激后细胞因子的释放。方法：雄性ApoE(-/-)小鼠暴露于SDR应激12周，测量动脉、主动脉根部和无名动脉的动脉粥样硬化斑块面积。进一步，雄性C57BL/6小鼠暴露于SDR应激或5种物理应激源，并在应激后即刻检测血浆/血清中细胞因子和皮质酮的水平。结果：SDR应激水平与主动脉粥样硬化斑块面积和主动脉根部斑块面积的数值增加存在相关性。SDR应激不影响斑块成分的组织学特征。然而，SDR应激增加了皮质酮、IL-6和CXCL1的水平。血浆皮质酮在所有五种物理应激源中均升高，但IL-6和CXCL1仅在暴露于束缚和老鼠气味的组中增加。结论：这些发现表明SDR应激确实是动脉粥样硬化的致病因素，与我们之前使用物理应激源的结果相反。这种差异的一个可能解释是SDR压力，而不是身体应激源，导致促炎细胞因子IL-6和CXCL1的释放。(C)2011爱思唯尔爱尔兰有限公司。保留所有权利。
Introduction: We have previously shown that different forms of stress have distinctive effects on atherogenesis in mice. We showed that social stress increase atherosclerosis in ApoE(-/-) mice, while more physical forms of stress do not. Here we evaluated the effect of social disruption (SDR) stress on atherogenesis and evaluated cytokine release after SDR-stress and five more physical stressors.Methods: Male ApoE(-/-) mice were exposed to SDR-stress during 12 weeks, and atherosclerotic plaque area was assessed in aorta, aortic root and innominate artery. Further, male C57BL/6 mice were exposed to SDR-stress or five physical stressors, and cytokine and corticosterone levels were analyzed in plasma/serum samples immediately after stress.Results: We found a correlation between the level of SDR-stress and atherosclerotic plaque area in aorta and a numerical increased plaque area in aortic root. SDR stress did not affect histological features of plaque composition. However, SDR-stress increased levels of corticosterone, IL-6 and CXCL1. Plasma corticosterone increased for all five physical stressors, but IL-6 and CXCL1 only increased in the group exposed to restraint combined with rat odor.Conclusions: These findings suggest that SDR-stress is indeed atherogenic, in contrast to our previous results using the physical stressors. A possible explanation to this difference is that SDR-stress, but not physical stressors, leads to release of the pro-inflammatory cytokines IL-6 and CXCL1. (C) 2011 Elsevier Ireland Ltd. All rights reserved.