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白三烯B4体内脱敏对豚鼠皮肤中嗜酸性粒细胞因C5a产生浸润的影响。

Effect of in vivo desensitization to leukotriene B4 on eosinophil infiltration in response to C5a in guinea-pig skin.

作者信息

Pettipher E R, Salter E D, Showell H J

机构信息

Department of Immunology and Infectious Diseases, Pfizer Inc., Groton, CT 06340.

出版信息

Br J Pharmacol. 1994 Sep;113(1):117-20. doi: 10.1111/j.1476-5381.1994.tb16182.x.

Abstract
  1. The effect of in vivo desensitization to leukotriene B4 (LTB4) on eosinophil infiltration in response to recombinant C5a was examined in guinea-pig skin. 2. LTB4 (10-300 ng) and C5a (1-10 micrograms) caused a dose-dependent increase in the levels of eosinophil peroxidase activity (a measure of eosinophil infiltration) 4 h after injection into guinea-pig skin. Leukotriene B4 and C5a were approximately equipotent on a molar basis. Platelet activating factor (0.01-10 micrograms) also caused eosinophil accumulation but was much less active than LTB4 or C5a. 3. 20-Hydroxy-LTB4 caused a dose-dependent desensitization of eosinophil responses to LTB4 (ED50 = 1.6 micrograms kg-1, s.c.) and partially reduced responses to C5a. At a dose of 20-hydroxy-LTB4 (10 micrograms) which inhibited responses to LTB4 completely, responses to C5a were reduced by 56.5 +/- 1.8% (n = 5). The structurally related metabolite of 20-hydroxy-LTB4, 20-carboxy-LTB4, which does not cause desensitization to the effects of LTB4, did not inhibit eosinophil infiltration in response to C5a. 4. The LTB4 receptor antagonist, SC-41,930 (10 mg kg-1, p.o.), also inhibited eosinophil accumulation in response to C5a by 63.0 +/- 3.9% (n = 5) at a dose which inhibited responses to LTB4 by 86.5 +/- 1.9% (n = 5). 5. These data indicate that eosinophil infiltration in response to C5a may, in part, be mediated by the generation of secondary chemotactic factors such as LTB4.
摘要
  1. 在豚鼠皮肤中研究了体内对白三烯B4(LTB4)脱敏对重组C5a诱导的嗜酸性粒细胞浸润的影响。2. 将LTB4(10 - 300 ng)和C5a(1 - 10μg)注射到豚鼠皮肤4小时后,嗜酸性粒细胞过氧化物酶活性水平(嗜酸性粒细胞浸润的一种测量指标)呈剂量依赖性增加。白三烯B4和C5a在摩尔基础上大致等效。血小板活化因子(0.01 - 10μg)也引起嗜酸性粒细胞聚集,但活性远低于LTB4或C5a。3. 20 - 羟基 - LTB4引起对LTB4的嗜酸性粒细胞反应的剂量依赖性脱敏(ED50 = 1.6μg kg-1,皮下注射),并部分降低对C5a的反应。在20 - 羟基 - LTB4剂量为10μg时,其完全抑制对LTB4的反应,对C5a的反应降低了56.5±1.8%(n = 5)。20 - 羟基 - LTB4的结构相关代谢物20 - 羧基 - LTB4不会引起对LTB4作用的脱敏,也不抑制对C5a的嗜酸性粒细胞浸润。4. LTB4受体拮抗剂SC - 41,930(10 mg kg-1,口服)在抑制对LTB4反应86.5±1.9%(n = 5)的剂量下,也将对C5a的嗜酸性粒细胞聚集抑制了63.0±3.9%(n = 5)。5. 这些数据表明,对C5a的嗜酸性粒细胞浸润可能部分由诸如LTB4等二级趋化因子的产生介导。

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The release of leukotriene B4 during experimental inflammation.实验性炎症过程中白三烯B4的释放。
Biochem Pharmacol. 1983 Apr 15;32(8):1353-9. doi: 10.1016/0006-2952(83)90446-x.

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