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在缺乏内皮氧化合成酶的小鼠中,脂肪条形成的悖论性减少

Weibin Shi¹, Xuping Wang, Diana M Shih

¹Department of Radiology and Cardiovascular Research Center (W.S.) and Surgery, University of Virginia, Charlottesville, Va, USA.

|May 1, 2002

概括

内皮氧化合成酶 (eNOS) 缺乏意想不到地减少了小鼠的饮食诱导的脂肪条纹形成. 这表明eNOS介导的LDL氧化有助于动脉样硬化发展.

科学领域:

心血管生物学心血管生物学
动脉样硬化研究动脉样硬化研究
分子医学是分子医学.

背景情况:

氧化物合成酶 (eNOS) 的内皮异型因氧化物 (NO) 合成而传统上被视为抗动脉样硬化剂.
然而,eNOS也可以产生超氧化物,可能会氧化LDL并促进动脉样硬化.
这项研究研究了eNOS在饮食诱导的脂肪条形形成中的作用,使用eNOS缺乏的小鼠.

研究的目的:

确定eNOS在饮食诱导的脂肪条纹病变的发展中的特定作用.
为了阐明eNOS是否有助于动脉壁内的LDL氧化.

主要方法:

缺乏eNOS和野生类型的小鼠被食了异质性饮食12周.
在大动脉根部的动脉样硬化病变使用油红色O染色量化.
隔离了内皮细胞,以评估在存在或缺乏NOS抑制剂 (L-NAME) 的情况下的LDL氧化.

主要成果:

与野生类型对照组相比,缺乏eNOS的小鼠表现出明显较小的大动脉病变 (P=0.03).
损伤大小的减少不能归因于血脂水平变化或脂蛋白氧化易感性.
L-NAME抑制了野生型内皮细胞的LDL氧化,但不是因ENOS缺乏细胞,这表明ENOS在这个过程中的作用.

结论:

没有eNOS介导的LDL氧化与减少脂肪条形形成有关.
这些发现表明,eNOS通过促进LDL氧化促进动脉样硬化.

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