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黄嘌呤衍生物对趋化多肽诱导的人多形核白细胞超氧化物和酶释放的影响。

Effect of xanthine derivatives on chemotactic polypeptide-induced superoxide and enzyme release from human polymorphonuclear leucocytes.

作者信息

Hirano T, Ando M, Suzuki K, Furui H, Miyamoto K, Takagi K

机构信息

Second Department of Internal Medicine, Nagoya University School of Medicine, Japan.

出版信息

Clin Exp Pharmacol Physiol. 1993 Sep;20(9):579-85. doi: 10.1111/j.1440-1681.1993.tb01744.x.

DOI:10.1111/j.1440-1681.1993.tb01744.x
PMID:8222338
Abstract
  1. We investigated the effects of new xanthine derivatives, 1-methyl-3-propyl xanthine (MPX) and 1,3-dipropyl xanthine (DPX), and several other xanthine derivatives on N-formyl-methionyl-leucyl-phenylalanine-induced superoxide and lysozyme release from human polymorphonuclear leucocytes (PMN). 2. MPX and DPX at low concentrations (10(-8) - 10(-9) mol/L) inhibited superoxide release from PMN by a maximum of 31.2 +/- 10.6% and 49.8 +/- 10.4% (mean +/- s.d.), respectively, and 10(-3) mol/L concentrations completely inhibited the release reactions (4.8 +/- 1.2 and 7.6 +/- 2.5% of control level). At 10(-5) mol/L, however, the inhibition did not occur (99.9 +/- 7.3 and 110.2 +/- 15.8% of control level). When PMN was pre-incubated with adenosine deaminase (ADA, 0.1 U/mL), superoxide release from PMN was inhibited in a dose-dependent manner by MPX and DPX and the interruption of the inhibition at 10(-5) mol/L was not observed. 3. Lysozyme release from PMN was inhibited by MPX at low concentrations (10(-7) - 10(-6) mol/L) and high concentrations (10(-3) mol/L). However 10(-4) mol/L of MPX facilitated the release (23.7 +/- 27.0%). When pretreated with ADA (0.1 U/mL), MPX suppressed lysozyme release in a dose-dependent manner and the facilitation of the release at 10(-4) mol/L was not observed. 4. When comparing effects of some other xanthine derivatives on superoxide release, the interruption of the inhibition of superoxide release at 10(-5) mol/L was commonly observed among xanthine derivatives with adenosine A2 antagonism.(ABSTRACT TRUNCATED AT 250 WORDS)
摘要
  1. 我们研究了新型黄嘌呤衍生物1-甲基-3-丙基黄嘌呤(MPX)和1,3-二丙基黄嘌呤(DPX)以及其他几种黄嘌呤衍生物对N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸诱导的人多形核白细胞(PMN)超氧化物释放和溶菌酶释放的影响。2. 低浓度(10⁻⁸ - 10⁻⁹mol/L)的MPX和DPX分别最大程度地抑制PMN超氧化物释放31.2±10.6%和49.8±10.4%(平均值±标准差),10⁻³mol/L浓度则完全抑制释放反应(为对照水平的4.8±1.2%和7.6±2.5%)。然而,在10⁻⁵mol/L时,抑制作用未出现(为对照水平的99.9±7.3%和110.2±15.8%)。当PMN与腺苷脱氨酶(ADA,0.1 U/mL)预孵育时,MPX和DPX以剂量依赖方式抑制PMN超氧化物释放,且未观察到在10⁻⁵mol/L时抑制作用的中断。3. 低浓度(10⁻⁷ - 10⁻⁶mol/L)和高浓度(10⁻³mol/L)的MPX抑制PMN溶菌酶释放。然而,10⁻⁴mol/L的MPX促进了释放(23.7±27.0%)。当用ADA(0.1 U/mL)预处理时,MPX以剂量依赖方式抑制溶菌酶释放,且未观察到在10⁻⁴mol/L时释放的促进作用。4. 当比较其他一些黄嘌呤衍生物对超氧化物释放的影响时,在具有腺苷A2拮抗作用的黄嘌呤衍生物中普遍观察到在10⁻⁵mol/L时超氧化物释放抑制作用的中断。(摘要截断于250字)

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