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首页> 外文期刊>FEBS Letters >Effect of leukotriene B4, prostaglandin E2 and arachidonic acid on cytosolic‐free calcium in human neutrophils
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Effect of leukotriene B4, prostaglandin E2 and arachidonic acid on cytosolic‐free calcium in human neutrophils

机译:白三烯B4,前列腺素E2和花生四烯酸对人中性粒细胞中无钙质钙的影响

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>Changes in cytosolic free calcium [Ca2+]i and release of beta-glucuronidase in response to leukotriene B4 (LTB4) were measured in intact neutrophils loaded with the fluorescent Ca2+ indicator, quin 2. LTB4 (10−10 M or higher) caused a rapid rise in [Ca2+]i due to influx from the extracellular medium and release from intracellular pools as well as enzyme release. PGE2 (3 μM) did not alter [Ca2+]i whereas arachidonic acid (10 μM) raised [Ca2+]i. Pretreatment of cells with the chemotactic peptide FMLP inhibited the subsequent rise of [Ca2+]i induced by LTB4. Since chemotactic peptides activate the lipoxygenase pathway of arachidonic acid metabolism, it may be speculated that endogenous LTB4 generation is involved in neutrophil activation.
机译:>对白三烯B 4 的响应(LTB <,细胞内游离钙[Ca 2 + ] i 的变化和β-葡萄糖醛酸苷酶的释放在装有荧光Ca 2 + 指示剂quin 2的完整嗜中性白细胞中测量了sub> 4 )。LTB 4 (10 −10 M或更高)导致[Ca 2 + ] i 迅速上升,这是由于从细胞外培养基中流入并从细胞内池中释放以及酶释放。 PGE 2 (3μM)没有改变[Ca 2 + ] i ,而花生四烯酸(10μM)升高了[Ca 2 + ] i 。用趋化肽FMLP预处理细胞可抑制LTB 4 诱导的[Ca 2 + ] i 随后的升高。由于趋化肽激活花生四烯酸代谢的脂氧合酶途径,因此可以推测内源性LTB 4 的产生与嗜中性粒细胞的激活有关。

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