物质P-induced cyclooxygenase-2人类脐静脉内皮细胞表达。

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Gallicchio M,罗莎交流,他E, Collino M, Dianzani C, Fantozzi R

物质P-induced cyclooxygenase-2人类脐静脉内皮细胞表达。

Br J杂志。2006年3月,147 (6):681 - 9。

PubMed ID

16432508 (在PubMed

]

文摘

P物质(SP)是一种神经肽参与神经源性炎症和NK(1)受体激动剂,NK (2), NK(3)受体。SP诱发前列腺素(PG)生产在不同的细胞类型,这类花生酸负责许多炎症和血管的影响。环氧合酶(COX)需要将花生四烯酸转化为动力。研究评价SP对考克斯的影响表现在人类脐静脉内皮细胞(HUVEC)。cox - 2蛋白表达的调节是SP与峰值在100 nM和20 h;在相同的实验条件COX-1蛋白表达是不变。cox - 2表达之间的相关性和PGI(2)和铂族元素(2)释放检测。地塞米松(DEX)抑制SP-mediated cox - 2的表达。增殖蛋白激酶(MAPK) p38和SP p42/44被激活,而SB202190 PD98059,这些激酶的抑制剂,阻止了cox - 2的表达。(5,5-dimethyl-3) - 3-fluorophenyl 4 - (4-methylsulphonyl) phenyl-2 (5 h) -furanone (DFU),一个实验性的选择性cox - 2抑制剂,阻塞SP-induced PG释放。 By RT-PCR and Western blot analysis, we demonstrated that NK(1) and NK(2) but not NK(3) receptors are present on HUVEC. Selective NK(1) and NK(2) agonists, namely [Sar(9), Met(O(2))(11)]SP and [beta-Ala(8)] NKA(4-10), upregulated COX-2 protein expression and PG production, whereas senktide (Suc-Asp-Phe-MePhe-Gly-Leu-Met-NH(2)), a selective NK(3) agonist, was ineffective in this respect. The NK(1) selective antagonist L703,606 ((cis)-2-(diphenylmethyl)-N-((2-iodophenyl)-methyl)-1-azabicyclo(2.2.2)octan-3-am ine) and the NK(2) selective antagonist SR 48,968 ((S)-N-methyl-N-(4-(4-acetylamino-4-phenylpiperidino)-2-(3,4 dichlorophenyl)butyl) benzamide) competitively antagonised SP-induced effects. The study shows HUVEC to possess functional NK(1) and NK(2) receptors, which mediate the ability of SP to induce expression of COX-2 in HUVEC, thus showing a previously-undetected effect of SP on endothelial cells.

DrugBank数据引用了这篇文章

药物酶

药物	酶	类	生物	药理作用	行动
Sar9 (O2) 11-Substance P相遇	前列腺素合成酶2 G / H	蛋白质	人类	未知的	诱导物	细节