Eicosapentaenoic acid potentiates the production of nitric oxide evoked by interleukin-1 beta in cultured vascular smooth muscle cells.

Eicosapentaenoic acid potentiates the production of nitric oxide evoked by interleukin-1 beta in cultured vascular smooth muscle cells.
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二十碳五烯酸可增强培养的血管平滑肌细胞中白介素 1 β 引起的一氧化氮的产生。

DOI:
10.1159/000158996
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发表时间:
1993
影响因子:
1.7
通讯作者:
Vanhoutte,PM
Vanhoutte,PM
中科院分区:
医学4区
文献类型:
--
作者:
Schini,VB;Durante,W;Catovsky,S;Vanhoutte,PM

文献摘要

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设计实验以确定ω3-不饱和脂肪酸二十碳五烯酸是否影响培养的血管平滑肌细胞中由白细胞介素-1β引起的一氧化氮的产生。将培养的大鼠或人主动脉平滑肌细胞与白细胞介素-1β一起孵育,会引起亚硝酸盐(一氧化氮的氧化产物)的时间和浓度依赖性释放。将细胞暴露于白细胞介素-1β与二十碳五烯酸的组合中,比单独使用细胞因子引起的亚硝酸盐产生量显着增加。二十碳五烯酸的增强作用是浓度依赖性的。在存在或不存在二十碳五烯酸的情况下,等有效浓度的白细胞介素-1β引起的亚硝酸盐的产生受到硝基L-精氨酸(一氧化氮合酶的抑制剂)、转化生长因子β1、血小板衍生生长因子AB和凝血酶的类似程度的抑制。将白细胞介素-1β激活的平滑肌细胞添加到洗涤的和吲哚美辛处理的血小板的悬浮液中抑制了凝血酶引起的聚集。当实验前将平滑肌细胞在二十碳五烯酸存在下暴露于细胞因子时,抑制效果增强。在氧合血红蛋白或亚甲蓝存在的情况下,暴露于白细胞介素-1β和二十碳五烯酸的平滑肌细胞不会影响血小板聚集。未经处理的细胞或单独暴露于脂肪酸的细胞不具有这样的效果。这些观察结果表明,二十碳五烯酸可增强血管平滑肌中白细胞介素-1β 引起的一氧化氮的产生。
Experiments were designed to determine whether the ω3-unsaturated fatty acid eicosapentaenoic acid affects the production of nitric oxide evoked by interleukin-lβ in cultured vascular smooth muscle cells. Incubation of cultured rat or human aortic smooth muscle cells with interleukin-1β evoked a time- and concentration-dependent release of nitrite, an oxidation product of nitric oxide. The exposure of cells to interleukin-1β in combination with eicosapentaenoic acid caused a significantly larger production of nitrite than that evoked by the cytokine alone. The potentiation by eicosapentaenoic acid was concentration-dependent. The production of nitrite evoked by equieffective concentrations of interleukin-1β in the presence and absence of eicosapentaenoic acid were inhibited to a similar extent by nitro L-arginine (an inhibitor of nitric oxide synthase), transforming growth factor β1platelet-derived growth factorABand thrombin. The addition of interleukin-1β -activated smooth muscle cells to suspensions of washed and indomethacin-treated platelets inhibited the aggregation caused by thrombin. The inhibitory effect was enhanced when the smooth muscle cells were exposed to the cytokine in the presence of eicosapentaenoic acid prior to the experiment. Smooth muscle cells exposed to interleukin-1β and eicosapentaenoic acid did not affect platelet aggregation in the presence of oxyhemoglobin or methylene blue. Untreated cells or cells exposed to the fatty acid alone did not have such effects. These observations suggest that eicosapentaenoic acid potentiates the production of nitric oxide evoked by interleukin-1β in vascular smooth muscle.