Effect of lysophosphatidylcholine on vasomotor functions of porcine coronary arteries.
Effect of lysophosphatidylcholine on vasomotor functions of porcine coronary arteries.
复制标题
溶血磷脂酰胆碱对猪冠状动脉血管舒缩功能的影响。
DOI：
10.1016/j.jss.2005.01.015
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发表时间：
2005
期刊：
影响因子：
--
通讯作者：
Chen,Changyi
中科院分区：
文献类型：
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作者：
Safaya,Rakesh;Chai,Hong;Kougias,Panagiotis;Lin,Peter;Lumsden,Alan;Yao,Qizhi;Chen,Changyi
背景溶血磷脂酰胆碱(LPC)是磷脂酶A2水解磷脂酰胆碱的产物，是脂质诱导的动脉粥样硬化变化的介质。在这项研究中，我们确定了LPC对猪冠状动脉血管舒缩功能、氧化应激和内皮一氧化氮合酶（eNOS）表达的影响。方法将猪冠状动脉切成5毫米的环，并用LPC或抗氧化剂硒代蛋氨酸（SeMet）处理。对于血管舒缩研究，我们使用肌动描记器张力系统。通过光泽精增强化学发光法检测超氧阴离子 (O2−) 水平。使用亲和素-生物素复合物免疫过氧化物酶程序通过免疫组织化学研究 eNOS 蛋白水平。结果与对照组相比，用 12.5 μm 和 25 μm LPC 处理的环对缓激肽反应的内皮依赖性松弛分别降低了 36% 和 81%（P < 0.05）。用 25 μm LPC 治疗后，硝普钠反应的内皮依赖性舒张也减少了 63%（P < 0.05）。与对照组相比，用 25 μm LPC 处理的猪动脉中的 O2−水平增加了 41%（P < 0.05）。抗氧化剂 SeMet 逆转了 LPC 对血管松弛和 O2 产生的影响。 LPC处理的血管环中eNOS的免疫反应性也显着降低。结论SLPC损害内皮依赖性和内皮非依赖性血管舒张。这种效应与超氧自由基产生增加和 eNOS 活性降低有关，并且实际上可以通过使用抗氧化剂 SeMet 来逆转。
BACKGROUNDLysophosphatidylcholine (LPC) is a product of phosphatidylcholine hydrolysis by phospholipase A2and a mediator of the lipid-induced atherosclerotic changes. In this study, we determined the effects of LPC on vasomotor functions, oxidative stress, and endothelial nitric oxide synthase (eNOS) expression in porcine coronary arteries.METHODSPorcine coronary arteries were cut into 5-mm rings and were treated with LPC or antioxidant selenomethionine (SeMet). For the vasomotor studies, we used a myograph tension system. Levels of superoxide anion (O2−) were detected by the lucigenin-enhanced chemiluminescence method. The eNOS protein level was studied by immunohistochemistry with avidin-biotin complex immunoperoxidase procedure.RESULTSEndothelium-dependent relaxation in response to bradykinin was reduced by 36% and 81% for the rings treated with 12.5 and 25 μm of LPC, respectively, as compared with controls (P < 0.05). Endothelium-independent relaxation in response to sodium nitroprusside also was reduced by 63% after treatment with 25 μm LPC (P < 0.05). The O2−level was increased in the porcine arteries treated with 25 μm of LPC by 41% as compared with controls (P < 0.05). The antioxidant SeMet reversed the effects of LPC on vascular relaxation and O2−production. Immunoreactivity of eNOS in LPC-treated vessel rings also was reduced substantially.CONCLUSIONSLPC impairs endothelium-dependent and endothelium-independent vasorelaxation. This effect is associated with increased superoxide radical production and decreased eNOS activity and is practically reversed with the use of the antioxidant SeMet.