Lysophosphatidylcholine (LPC) attenuates macrophage-mediated oxidation of LDL
Lysophosphatidylcholine (LPC) attenuates macrophage-mediated oxidation of LDL
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DOI：
10.1016/j.bbrc.2006.04.038
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发表时间：
2006-06-16
影响因子：
3.1
通讯作者：
Aviram, Michael
中科院分区：
文献类型：
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作者：
Rosenblat, Mira;Oren, Roni;Aviram, Michael
我们之前已经证明，对氧磷酶1作用于巨噬细胞产生溶血磷脂酰胆碱（LPC），并显著降低细胞介导的LDL氧化。因此，在本研究中，我们质疑LPC是否可以直接抑制巨噬细胞介导的LDL氧化。在J774A.1巨噬细胞、小鼠腹膜巨噬细胞（MPM）或人单核细胞源性巨噬细胞（HMDM）中添加增加LPC浓度（0-5 μ M），可分别抑制高达83%、67%和75%的细胞介导的LDL氧化。这种LPC效应的机制包括：响应于磷脂酯（PMA）的MPNI超氧阴离子释放抑制高达60%，PMA诱导的NADPH氧化酶激活抑制26% （p47phox从细胞质溶胶转移到质膜），以及巨噬细胞对氧磷酶2 （PON2）内酯酶活性的2倍刺激。因此，我们得出结论，LPC抑制巨噬细胞介导的LDL氧化有助于抑制巨噬细胞泡沫细胞的形成和动脉粥样硬化病变的发展。(c) 2006爱思唯尔公司版权所有。
We have previously shown that paraoxonase 1 action on macrophages produced lysophosphatidylcholine (LPC) and significantly decreased cell-mediated LDL oxidation. Thus, in the present study, we questioned whether LPC can directly inhibit macrophage-mediated oxidation of LDL. Addition of increasing LPC concentrations (0-5 mu M) to J774A.1 macrophages, mouse peritoneal macropliages (MPM), or to human monocytes-derived macrophages (HMDM) resulted in up to 83%, 67%, and 75% inhibition in cell-mediated oxidation of LDL, respectively. The mechanism for this LPC effect involves up to 60% inhibition of superoxide anion release from MPNI in response to phorbol ester (PMA), 26% inhibition of PMA-induced NADPH oxidase activation (p47phox translocation from the cytosol to the plasma membrane), and a 2-fold stimulation of the macrophage paraoxonase 2 (PON2) lactonase activity. We thus conclude that inhibition of macrophage-mediated oxidation of LDL by LPC can contribute to attenuation of macrophage foam cell formation and atherosclerotic lesion development. (c) 2006 Elsevier Inc. All rights reserved.