دورية أكاديمية
Atherosclerotic plaque disruption induced by stress and lipopolysaccharide in apolipoprotein E knockout mice.
| العنوان: | Atherosclerotic plaque disruption induced by stress and lipopolysaccharide in apolipoprotein E knockout mice. |
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| المؤلفون: | Mei Ni, Yan Wang, Mei Zhang, Peng Fei Zhang, Shi Fang Ding, Chun Xi Liu, Xiao Ling Liu, Yu Xia Zhao, Yun Zhang |
| المصدر: | American Journal of Physiology: Heart & Circulatory Physiology; May2009, Vol. 296 Issue 5, pH1598-H1606, 9p |
| مصطلحات موضوعية: | ATHEROSCLEROTIC plaque, EFFECT of stress on animals, ENDOTOXINS, APOLIPOPROTEIN E genetics, POLYSACCHARIDES, HEMODYNAMICS, LABORATORY mice |
| مستخلص: | Ni M, Wang Y, Zhang M, Zhang PF, Ding SF, Liu CX, Liu XL, Zhao YX, Zhang Y. Atherosclerotic plaque disruption induced by stress and lipopolysaccharide in apolipoprotein E knockout mice. Am J Physiol Heart Circ Physiol 296: H1598-H1606, 2009. First published March 13, 2009; doi: 10.1 152/ajpheart.0 1202.2008.-To establish an animal model with disruptions of atherosclerotic plaques, 96 male apolipoprotein E knockout (apoE) mice were randomly divided into stress, lipopolysaccharide (LPS), stress+LPS, and control groups (n = 24 each). All mice were fed a high-fat diet throughout the experiment, and carotid atherosclerotic lesions were induced by placement of a constrictive perivascular collar. Four weeks after surgery, mice in the LPS and stress+LPS groups were intraperitoneally injected with LPS (1 mg/kg twice per week for 8 wk). Eight weeks after surgery, mice in the stress and stress+LPS grOups were treated with intermittent physical stress (electric foot shock and noise stimulation) for 4 wk. Morphological analysis revealed a plaque disruption rate of 16.7% in control, 34.8% in LPS, 54.2% in stress, and 60.9% in stress+LPS groups. The disruption rates in stress and stress+LPS groups were both significantly higher than those of controls (P = 0.007 and P = 0.002, respectively). Luminal thrombosis secondary to plaque disruption was observed only in the stress+LPS group. Both stress and LPS stimulation significantly decreased fibrous cap thickness and increased macrophage and lipid contents in plaques. Moreover, the combination of stress and LPS stimulation further lowered cap thickness and enhanced accumulation of macrophages and expression of inflammatory cytokines and matrix metalloproteinases. Stress activated the sympathetic nervous system, as manifested by increased blood pressure and flow velocity. Plasma fibrinogen levels were remarkably elevated in the stress and stress+LPS groups. In conclusion, stressand LPS-costimulated apoE[sup-/-] mice provide a useful model for studies of plaque vulnerability and interventions. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: | Complementary Index |
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