在组胺释放过程中，抗过敏剂NCO-650对磷脂甲基化的抑制作用。
Inhibition of phospholipid methylation by an anti-allergic agent, NCO-650, during histamine release.
作者信息
Takei M, Matumoto T, Endo K, Muramatu M
机构信息
Department of Pharmacology, Tokushima Bunri University, Japan.
出版信息
Biochem Pharmacol. 1990 Oct 15;40(8):1773-8. doi: 10.1016/0006-2952(90)90355-o.
Antigen, anti-IgE and concanavalin A (Con A) induced an increase in both the incorporation of the 3H-methyl moiety into phospholipids and histamine release. Maximal incorporation of the 3H-methyl moiety into the lipid fraction of the cells was observed within 15 sec and 1 min after being challenged with antigen (100 micrograms/mL) and anti-IgE (200 micrograms/mL) respectively. However, the methylated phospholipid decreased rapidly. The addition of Con A (10 micrograms/mL) also increased phospholipid methylation, which reached a maximum at 5 min after challenge. Trans-4-guanidinomethylcyclohexanecarboxylic acid p-tert-butylphenyl ester hydrochloride (NCO-650; 27 microM) strongly inhibited the incorporation of the 3H-methyl moiety into phospholipid by antigen, anti-IgE and Con A. The IC50 values of NCO-650 for phospholipid methylation in response to antigen, anti-IgE and Con A were 1.5, 4.7 and 1.1 microM respectively. Although the Ca2(+)-ionophore A23187 did not induce phospholipid methylation, it caused histamine release.
抗原、抗IgE和伴刀豆球蛋白A（Con A）均能诱导3H-甲基部分掺入磷脂以及组胺释放增加。在用抗原（100微克/毫升）和抗IgE（200微克/毫升）分别刺激后，在15秒和1分钟内观察到3H-甲基部分最大程度地掺入细胞的脂质部分。然而，甲基化磷脂迅速减少。添加Con A（10微克/毫升）也会增加磷脂甲基化，在刺激后5分钟达到最大值。反式-4-胍基甲基环己烷羧酸对叔丁基苯基酯盐酸盐（NCO-650；27微摩尔）强烈抑制抗原、抗IgE和Con A诱导的3H-甲基部分掺入磷脂。NCO-650对抗原、抗IgE和Con A诱导的磷脂甲基化的IC50值分别为1.5、4.7和1.1微摩尔。尽管钙离子载体A23187不会诱导磷脂甲基化，但它会引起组胺释放。
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