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唾液酸或N - 乙酰葡糖胺特异性凝集素对化合物48/80、缓激肽和聚乙烯亚胺诱导大鼠腹膜肥大细胞组胺释放的抑制作用。

Inhibitory effects of sialic acid- or N-acetylglucosamine-specific lectins on histamine release induced by compound 48/80, bradykinin and a polyethylenimine in rat peritoneal mast cells.

作者信息

Matsuda K, Niitsuma A, Uchida M K, Suzuki-Nishimura T

机构信息

Department of Molecular Pharmacology, Meiji College of Pharmacy, Tokyo, Japan.

出版信息

Jpn J Pharmacol. 1994 Jan;64(1):1-8. doi: 10.1254/jjp.64.1.

DOI:10.1254/jjp.64.1
PMID:7513032
Abstract

The effects of seven lectins with various sugar-specificities on histamine release from rat peritoneal mast cells induced by non-immunologic stimuli were studied. The non-immunologic stimuli used were three basic secretagogues, compound 48/80, bradykinin and PEI6 (polyethylenimine with a molecular weight of 600). In this study, we observed inhibition of the histamine release by Macckia amurensis mitogen and Solanum tuberosum agglutinin (100 micrograms/ml at 37 degrees C for 10 min), which are specific for sialic acid-alpha 2,3-N-acetyl galactosamine (Sia alpha 2,3GalNAc) and N-acetyl glucosamine (GlcNAc) oligomers, respectively. The effects of Phytolacca americana mitogen and Sambucus sieboldiana agglutinin were different. Three lectins specific for mucin type oligosaccharides inhibited the histamine release induced by compound 48/80 but not that induced by bradykinin or PEI6. Since bradykinin and PEI6 additively enhanced the histamine release induced by compound 48/80, they partially shared the same signalling pathways. Glycoproteins with bisecting GlcNAc and Sia residues, as described previously (Jpn. J. Pharmacol. 57, 79-90, 1991), seemed to be one of the action sites for compound 48/80, bradykinin and PEI6. In addition to the direct activation of the pertussis toxin-sensitive G proteins, we propose another mechanism of non-immunologic stimuli via specific glycoproteins on rat peritoneal mast cells. The apparent sugar residues involved were asparagine-linked oligosaccharides with Sia (especially Sia alpha 2,3Gal), GlcNAc oligomers and/or bisecting GlcNAc.

摘要

研究了七种具有不同糖特异性的凝集素对非免疫刺激诱导的大鼠腹膜肥大细胞组胺释放的影响。所用的非免疫刺激物为三种基本促分泌剂,即化合物48/80、缓激肽和PEI6(分子量为600的聚乙烯亚胺)。在本研究中,我们观察到黑果枸杞有丝分裂原和马铃薯凝集素(37℃下100微克/毫升,作用10分钟)对组胺释放有抑制作用,它们分别对唾液酸-α2,3-N-乙酰半乳糖胺(Siaα2,3GalNAc)和N-乙酰葡糖胺(GlcNAc)寡聚物具有特异性。美洲商陆有丝分裂原和接骨木凝集素的作用不同。三种对粘蛋白型寡糖具有特异性的凝集素抑制了化合物48/80诱导的组胺释放,但不抑制缓激肽或PEI6诱导的组胺释放。由于缓激肽和PEI6可加性增强化合物48/80诱导的组胺释放,它们部分共享相同的信号通路。如先前所述(《日本药理学杂志》57, 79 - 90, 1991),具有平分型GlcNAc和Sia残基的糖蛋白似乎是化合物48/80、缓激肽和PEI6的作用位点之一。除了直接激活百日咳毒素敏感的G蛋白外,我们还提出了一种通过大鼠腹膜肥大细胞上的特异性糖蛋白进行非免疫刺激的机制。涉及的明显糖残基是带有Sia(尤其是Siaα2,3Gal)、GlcNAc寡聚物和/或平分型GlcNAc的天冬酰胺连接寡糖。

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