Nicotine stereoisomers and cotinine stimulate prostaglandin E2 but inhibit thromboxane B2 and leukotriene E4 synthesis in whole blood

Nicotine stereoisomers and cotinine stimulate prostaglandin E2 but inhibit thromboxane B2 and leukotriene E4 synthesis in whole blood
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DOI:
10.1016/s0014-2999(98)00384-7
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发表时间:
1998-07-17
影响因子:
5
通讯作者:
Riutta, A
Riutta, A
中科院分区:
医学2区
文献类型:
--
作者:
Saareks, V;Mucha, I;Riutta, A

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在体外Ca 2+离子载体A23187(卡西霉素)刺激的人全血中研究了(-)-尼古丁(0.0005 - 500 μ M)、(+)-尼古丁(0.0005 - 50 μ M)和(-)-可替宁(0.0005 - 500 μ M)对花生四烯酸代谢的影响。(-)-尼古丁和(-)-可替宁刺激前列腺素E-2,但抑制血栓烷B-2合成,如先前在A23187刺激的多形核白细胞和富血小板血浆中观察到的[Saareks,V.,Riutta,A.,穆查岛,Alanko,J.,Vapaatalo,H.,1993.尼古丁和可替宁调节人白细胞和富血小板血浆中类花生酸的产生。J. Pharmacol.,248,345 - 349.]。(+)-尼古丁也刺激前列腺素E-2,但抑制血栓素B-2的合成。高浓度的(-)-尼古丁和(-)-可替宁,甚至纳摩尔浓度的(+)-尼古丁抑制白三烯E-2的合成。这些结果表明,(-)-尼古丁和(-)-可替宁刺激环氧合酶,但抑制血栓素合酶和5-脂氧合酶在体外全血。(+)-尼古丁也能产生相同的影响。(C)1998 Elsevier Science B.V.保留所有权利。
The effects of (-)-nicotine (0.0005-500 mu M), (+)-nicotine (0.0005-50 mu M) and (-)-cotinine (0.0005-500 mu M) on arachidonic acid metabolism were investigated in Ca2+ ionophore A23187 (calcimycin)-stimulated human whole blood in vitro. (-)-Nicotine and (-)-cotinine stimulated prostaglandin E-2 but inhibited thromboxane B-2 synthesis, as has been observed previously in A23187-stimulated polymorphonuclear leukocytes and platelet-rich plasma [Saareks, V., Riutta, A., Mucha, I., Alanko, J., Vapaatalo, H., 1993. Nicotine and cotinine modulate eicosanoid production in human leukocytes and platelet rich plasma, fur. J. Pharmacol., 248, 345-349.]. (+)-Nicotine also stimulated prostaglandin E-2 but inhibited thromboxane B-2 synthesis. High concentrations of(-)-nicotine and(-)-cotinine and even nanomolar concentrations of (+)-nicotine inhibited leukotriene E-2 synthesis. These results indicate that (-)-nicotine and (-)-cotinine stimulate cyclooxygenase but inhibit thromboxane synthase and 5-lipoxygenase in whole blood in vitro. (+)-Nicotine is capable of affecting in the same direction as well. (C) 1998 Elsevier Science B.V. All rights reserved.