Bouchelouche P N, Ahnfelt-Rønne I, Thomsen M K
Dept. of Clinical Chemistry and Medical Gastroenterology, Copenhagen University Hospital, Herlev, Denmark.
Agents Actions. 1990 Mar;29(3-4):299-307. doi: 10.1007/BF01966461.
LTD4 increased the level of free intracellular calcium ([Ca++]i) and stimulated the production of inositol phosphates (IP) in human polymorphonuclear neutrophils (PMN). Calcium was predominantly mobilized from intracellular pools. After a single stimulus, the cells were refractory to a second challenge with the same concentration of LTD4, but the calcium response to LTB4 was normal. The rise in [Ca++]i as well as the stimulated production of IP was inhibited by the novel LTD4 antagonist, SR2640. SR2640 also abolished the attenuation by LTD4 of LTB4-directed PMN chemotaxis. The results suggest that human PMN contain specific LTD4 receptor that trigger phosphatidyl inositol hydrolysis by activation of phospholipase C, leading to intracellular calcium mobilization, which may be involved in modulation of chemotaxis.
白三烯D4（LTD4）可提高人多形核中性粒细胞（PMN）细胞内游离钙（[Ca++]i）水平，并刺激肌醇磷酸（IP）生成。钙主要从细胞内池释放。单次刺激后，细胞对相同浓度的LTD4再次刺激产生不应性，但对白三烯B4（LTB4）的钙反应正常。新型LTD4拮抗剂SR2640可抑制[Ca++]i升高以及IP生成增加。SR2640还消除了LTD4对LTB4介导的PMN趋化性的减弱作用。结果表明，人PMN含有特异性LTD4受体，该受体通过激活磷脂酶C触发磷脂酰肌醇水解，导致细胞内钙释放，这可能参与趋化性调节。
