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通过补体受体阻断抑制巨噬细胞中的呼吸爆发。

Inhibition of respiratory burst in macrophages by complement receptor blockade.

作者信息

Klegeris A, McGeer P L

机构信息

Kinsmen Laboratory of Neurological Research, Department of Psychiatry, University of British Columbia, Vancouver, Canada.

出版信息

Eur J Pharmacol. 1994 Aug 1;260(2-3):273-7. doi: 10.1016/0014-2999(94)90351-4.

Abstract

Respiratory burst activity was induced in rat peritoneal macrophages by opsonized zymosan. Inhibitors were tested by administering them before or after the inducing agent: OX-42, an anti-rat macrophage complement receptor type 3 antibody, was active at an estimated concentration of 2.1 nM, and was more than 100-fold more potent when administered before, rather than after, opsonized zymosan. Indomethacin and dapsone, two agents with antiinflammatory activity, were also more effective before opsonized zymosan, but only in the 10(-3) to 10(-4) molar range. Inhibitors of eicosanoid synthesis, as well as the antiinflammatory prostaglandin E2, also reduced the respiratory burst.

摘要

经调理的酵母聚糖可诱导大鼠腹腔巨噬细胞产生呼吸爆发活性。通过在诱导剂之前或之后给予抑制剂来进行测试:OX - 42,一种抗大鼠巨噬细胞3型补体受体抗体,在估计浓度为2.1 nM时具有活性,并且在经调理的酵母聚糖之前而非之后给药时,其效力要强100倍以上。消炎痛和氨苯砜这两种具有抗炎活性的药物,在经调理的酵母聚糖之前给药时也更有效,但仅在10⁻³至10⁻⁴摩尔范围内。类花生酸合成抑制剂以及抗炎性前列腺素E2也能降低呼吸爆发。

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