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脂氧素可刺激人内皮细胞生成前列环素。

Lipoxins stimulate prostacyclin generation by human endothelial cells.

作者信息

Brezinski M E, Gimbrone M A, Nicolaou K C, Serhan C N

机构信息

Department of Medicine, Brigham and Women's Hospital, Boston, MA.

出版信息

FEBS Lett. 1989 Mar 13;245(1-2):167-72. doi: 10.1016/0014-5793(89)80214-5.

DOI:10.1016/0014-5793(89)80214-5
PMID:2494071
Abstract

Cultured human umbilical endothelial cells were incubated with lipoxins and their ability to generate prostacyclin (PGI2) was assessed and compared to that induced by either leukotriene C4 or an ionophore of divalent cations (A-23,187). When exposed to either lipoxin A4, lipoxin B4, or 7-cis,11-trans-lipoxin A4, endothelial cells generated prostacyclin detected as 6-keto-PGF1 alpha. Of the lipoxins examined, 7-cis,11-trans-lipoxin A4 proved to be the most effective with PGI2 production twice that induced by equimolar amounts of A-23,187 (5 microM). On a molar basis, lipoxin A4 and lipoxin B4 were less potent than leukotriene C4 although they were more efficacious. When either lipoxin A4 or lipoxin B4 was added to cells simultaneously with leukotriene C4, the formation of prostacyclin was greater than that induced by leukotriene C4 alone. During the time course of exposure to lipoxins (0-20 min, 37 degrees C), cultured endothelial cells did not further transform these compounds via omega-oxidation as determined by reverse-phase HPLC. These data indicate that lipoxins can stimulate PGI2 generation by human endothelial cells. Moreover, they suggest a role for these lipoxygenase products of arachidonic acid in the regulation of hemostasis, inflammation and vascular reactivity.

摘要

将培养的人脐静脉内皮细胞与脂氧素一起孵育,评估其生成前列环素(PGI2)的能力,并与白三烯C4或二价阳离子载体(A - 23187)诱导的能力进行比较。当暴露于脂氧素A4、脂氧素B4或7 - 顺式,11 - 反式 - 脂氧素A4时,内皮细胞生成的前列环素可检测为6 - 酮 - PGF1α。在所检测的脂氧素中,7 - 顺式,11 - 反式 - 脂氧素A4被证明是最有效的,其PGI2生成量是等摩尔量的A - 23187(5 microM)诱导量的两倍。以摩尔为基础,脂氧素A4和脂氧素B4的效力低于白三烯C4,尽管它们更有效。当脂氧素A4或脂氧素B4与白三烯C4同时添加到细胞中时,前列环素的形成大于单独由白三烯C4诱导的形成。在暴露于脂氧素的时间过程中(0 - 20分钟,37℃),通过反相高效液相色谱法测定,培养的内皮细胞没有通过ω - 氧化进一步转化这些化合物。这些数据表明脂氧素可以刺激人内皮细胞生成PGI2。此外,它们提示这些花生四烯酸的脂氧合酶产物在止血、炎症和血管反应性调节中起作用。

相似文献

1
Lipoxins stimulate prostacyclin generation by human endothelial cells.脂氧素可刺激人内皮细胞生成前列环素。
FEBS Lett. 1989 Mar 13;245(1-2):167-72. doi: 10.1016/0014-5793(89)80214-5.
2
On the mechanism of transcellular lipoxin formation in human platelets and granulocytes.关于人血小板和粒细胞中跨细胞脂氧素形成的机制
Eur J Biochem. 1991 Jul 15;199(2):401-9. doi: 10.1111/j.1432-1033.1991.tb16137.x.
3
Lipoxin A4 and B4 inhibit leukotriene-stimulated interactions of human neutrophils and endothelial cells.脂氧素A4和B4可抑制白三烯刺激的人中性粒细胞与内皮细胞的相互作用。
J Immunol. 1996 Mar 15;156(6):2264-72.
4
Lipoxin A4 and lipoxin B4 stimulate the release but not the oxygenation of arachidonic acid in human neutrophils: dissociation between lipid remodeling and adhesion.脂氧素A4和脂氧素B4刺激人中性粒细胞中花生四烯酸的释放,但不影响其氧化:脂质重塑与黏附之间的分离。
J Cell Physiol. 1990 Jun;143(3):512-23. doi: 10.1002/jcp.1041430316.
5
Protein kinase C-regulated production of prostacyclin by rat endothelium is increased in the presence of lipoxin A4.在脂氧素A4存在的情况下,蛋白激酶C调节的大鼠内皮细胞前列环素生成增加。
FEBS Lett. 1990 Apr 9;263(1):117-20. doi: 10.1016/0014-5793(90)80718-x.
6
Lipoxins A4 and B4 inhibit leukotriene B4 generation from human neutrophil leukocyte suspensions.脂氧素A4和B4抑制人中性粒细胞悬液中白三烯B4的生成。
Immunol Lett. 1990 Jul;24(4):237-42. doi: 10.1016/0165-2478(90)90005-b.
7
Inhibition of leukotriene B4 in neutrophils by lipoxins A4 and B4.脂氧素A4和B4对中性粒细胞中白三烯B4的抑制作用。
Agents Actions. 1991 Jan;32(1-2):85-7. doi: 10.1007/BF01983321.
8
Conversion of 5,6-dihydroxyeicosatetraenoic acids. A novel pathway for lipoxin formation by human platelets.5,6-二羟基二十碳四烯酸的转化。人血小板形成脂氧素的一条新途径。
FEBS Lett. 1992 Jun 8;304(1):78-82. doi: 10.1016/0014-5793(92)80593-6.
9
Synthesis and metabolism of leukotrienes by human endothelial cells: influence on prostacyclin release.人内皮细胞白三烯的合成与代谢:对前列环素释放的影响。
Biochim Biophys Acta. 1988 Jun 15;960(3):309-21. doi: 10.1016/0005-2760(88)90039-2.
10
New series of lipoxins isolated from human eosinophils.从人嗜酸性粒细胞中分离出的新系列脂氧素。
FEBS Lett. 1989 Sep 11;255(1):143-8. doi: 10.1016/0014-5793(89)81078-6.

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