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一氧化碳在大鼠肺泡巨噬细胞鲁米诺依赖性化学发光中的作用。

The role of carbon monoxide in lucigenin-dependent chemiluminescence of rat alveolar macrophages.

作者信息

Fukushima T, Okinaga S, Sekizawa K, Ohrui T, Yamaya M, Sasaki H

机构信息

Department of Geriatric Medicine, Tohoku University School of Medicine, Sendai, Japan.

出版信息

Eur J Pharmacol. 1995 Mar 15;289(1):103-7. doi: 10.1016/0922-4106(95)90174-4.

DOI:10.1016/0922-4106(95)90174-4
PMID:7781703
Abstract

We have investigated the role of carbon monoxide (CO) in lucigenin-dependent chemiluminescence of alveolar macrophages from rat lungs. CO (10 nM to 1 microM) decreased chemiluminescence of alveolar macrophages in a concentration-dependent fashion. At a concentration of 1 microM, CO significantly increased intracellular cyclic GMP levels from a control value of 175 +/- 25 fmol/2 x 10(6) cells to 431 +/- 49 fmol/2 x 10(6) cells. Pretreatment of alveolar macrophages with NG-monomethyl-L-arginine (100 microM) failed to inhibit CO (1 microM)-induced decreases in chemiluminescence of alveolar macrophages (3.7 +/- 0.7 cpm x 10(3) in the presence of NG-monomethyl-L-arginine and 3.4 +/- 0.6 cpm x 10(3) in the absence of NG-monomethyl-L-arginine) and CO (1 microM)-induced increases in intracellular cyclic GMP levels (452 +/- 65 fmol/2 x 10(6) cells in the presence of NG-monomethyl-L-arginine and 419 +/- 58 fmol/2 x 10(6) cells in the absence of NG-monomethyl-L-arginine). Decreases in chemiluminescence of alveolar macrophages induced by CO (1 microM) were concentration-dependently inhibited by methylene blue (from 0.1 microM to 10 microM). Dibutyryl cyclic GMP (db cyclic GMP) (1 mM) also reduced chemiluminescence of alveolar macrophages (1.5 +/- 0.3 cpm x 10(3) in the presence of db cyclic GMP and 3.6 +/- 0.6 cpm x 10(3) in the absence of db cyclic GMP). In contrast to CO and db cyclic GMP, zinc protoporphyrin-9 (10nM to microM), an inhibitor of heme oxygenase potentiated chemiluminescence of alveolar macrophages in a concentration-dependent fashion.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

我们研究了一氧化碳(CO)在大鼠肺脏肺泡巨噬细胞的光泽精依赖性化学发光中的作用。CO(10 nM至1 microM)以浓度依赖性方式降低肺泡巨噬细胞的化学发光。在1 microM的浓度下,CO使细胞内环鸟苷酸水平从对照值175±25 fmol/2×10⁶个细胞显著增加至431±49 fmol/2×10⁶个细胞。用NG-单甲基-L-精氨酸(100 microM)预处理肺泡巨噬细胞未能抑制CO(1 microM)诱导的肺泡巨噬细胞化学发光降低(存在NG-单甲基-L-精氨酸时为3.7±0.7 cpm×10³,不存在时为3.4±0.6 cpm×10³)以及CO(1 microM)诱导的细胞内环鸟苷酸水平增加(存在NG-单甲基-L-精氨酸时为452±65 fmol/2×10⁶个细胞,不存在时为419±58 fmol/2×10⁶个细胞)。CO(1 microM)诱导的肺泡巨噬细胞化学发光降低可被亚甲蓝(浓度从0.1 microM至10 microM)浓度依赖性抑制。二丁酰环鸟苷酸(db环鸟苷酸)(1 mM)也降低了肺泡巨噬细胞的化学发光(存在db环鸟苷酸时为1.5±0.3 cpm×10³,不存在时为3.6±0.6 cpm×10³)。与CO和db环鸟苷酸相反,血红素加氧酶抑制剂锌原卟啉-9(10 nM至 microM)以浓度依赖性方式增强肺泡巨噬细胞的化学发光。(摘要截取自250字)

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