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氧化型低密度脂蛋白(OxLDL)诱导的细胞毒性及其在培养的猪主动脉内皮细胞中被API0134抑制的情况。

OxLDL-induced cytotoxicity and its inhibition by API0134 in cultured porcine aortic endothelial cells.

作者信息

Wang H, Zhao H, Ma B

机构信息

Department of Cardiology, Tongji Hospital, Tongji Medical University, Wuhan.

出版信息

J Tongji Med Univ. 1996;16(4):198-9, 202. doi: 10.1007/BF02888104.

DOI:10.1007/BF02888104
PMID:9389079
Abstract

Protective effects of API0134 on endothelial cells (EC) damaged by oxidatively modified low density lipoprotein (oxLDL) were studied. The results showed that the content of endothelia (ET) and malondialdehyde (MDA) in the media of porcine aortic EC incubated with oxLDL were increased and the cGMP was decreased significantly, and the activity of superoxide dismutase (SOD) was inhibited. The effect of cytotoxicity of oxLDL can be eliminated by API0134. These results suggest that API0134 may protect EC against damages elicited by oxLDL.

摘要

研究了API0134对氧化修饰低密度脂蛋白(oxLDL)损伤的内皮细胞(EC)的保护作用。结果显示,用oxLDL孵育的猪主动脉内皮细胞培养基中内皮素(ET)和丙二醛(MDA)含量增加,环磷酸鸟苷(cGMP)显著降低,超氧化物歧化酶(SOD)活性受到抑制。API0134可消除oxLDL的细胞毒性作用。这些结果提示,API0134可能保护内皮细胞免受oxLDL引起的损伤。

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OxLDL-induced cytotoxicity and its inhibition by API0134 in cultured porcine aortic endothelial cells.氧化型低密度脂蛋白(OxLDL)诱导的细胞毒性及其在培养的猪主动脉内皮细胞中被API0134抑制的情况。
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本文引用的文献

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The pathogenesis of atherosclerosis: a perspective for the 1990s.动脉粥样硬化的发病机制:20世纪90年代的展望
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