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缓激肽诱导小鼠纤维肉瘤中环状AMP积累,与前列腺素E2生成无关。

Bradykinin-induced cyclic AMP accumulation in mouse fibrosarcoma independent of prostaglandin E2 formation.

作者信息

Fujimoto M, Okabayashi T

出版信息

Jpn J Pharmacol. 1986 Jun;41(2):223-7. doi: 10.1254/jjp.41.223.

Abstract

The relationship between bradykinin (BK)-induced prostaglandin E2 (PGE2) and cyclic AMP syntheses in mouse fibrosarcoma cells (HSDM1C1) was investigated. Maximal BK-induced increases in cyclic AMP preceded increases in PGE2 production. PGE2 synthesis reached maximum at a much lower concentration of BK than cyclic AMP synthesis. Indomethacin completely inhibited BK-induced PGE2 production, but did not influence the cyclic AMP levels. Arachidonic acid in the medium induced PGE2 production in large quantities, but increased cyclic AMP accumulation only slightly. A high PGE2 concentration increased cyclic AMP levels only slightly. Theophylline increased basal and BK-mediated cyclic AMP levels, but did not affect PGE2 production at all. These results indicate that BK-evoked PGE2 and cyclic AMP syntheses in HSDM1C1 are not dependent upon each other.

摘要

研究了缓激肽(BK)诱导的前列腺素E2(PGE2)与小鼠纤维肉瘤细胞(HSDM1C1)中环磷酸腺苷(cAMP)合成之间的关系。BK诱导的cAMP最大增加先于PGE2产生的增加。PGE2合成在比cAMP合成低得多的BK浓度下达到最大值。吲哚美辛完全抑制BK诱导的PGE2产生,但不影响cAMP水平。培养基中的花生四烯酸大量诱导PGE2产生,但仅略微增加cAMP积累。高浓度的PGE2仅略微增加cAMP水平。茶碱增加基础和BK介导的cAMP水平,但对PGE2产生完全没有影响。这些结果表明,HSDM1C1中BK诱发的PGE2和cAMP合成并不相互依赖。

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