福多司坦对气道炎症导致的气管微血管血流增加的影响。
Effect of fudosteine, a cysteine derivative, on blood flow of tracheal microvasculature increased by airway inflammation.
机构信息
Central Research Laboratories, SS Pharmaceutical Co., Ltd., 1143 Nanpeidai, Narita 286-8511, Japan.
出版信息
Environ Toxicol Pharmacol. 2001 Jul;10(3):89-93. doi: 10.1016/s1382-6689(01)00075-8.
We examined the effect of fudosteine, a cysteine derivative, on blood flow of tracheal microvasculature increased by airway inflammation. Airway inflammation was elicited by sulfur dioxide (SO(2)) exposure for 2 weeks in rabbits. Each drug (500 mg/kg, p.o.) or 0.5% carboxymethylcellulose-Na (control group) was daily administered just before SO(2) exposure. After final SO(2) exposure was finished, blood flow of tracheal microvasculature was measured by blood perfusion monitor. Fudosteine or S-carboxymethylcysteine (S-CMC) significantly suppressed blood flow of tracheal microvasculature increased by SO(2) exposure. However, no effect of fudosteine was observed on the pharmacological microvascular response in trachea of SO(2)-exposed rabbits. On the other hand, fudosteine or S-CMC scavenged superoxide anion generated from rat neutrophils, and enzymatically generated from xanthine oxidase-acetaldehyde reaction. The results suggest that suppressive action in increased tracheal blood flow of fudosteine is due to anti-inflammatory activity, at least in part, via scavenging of superoxide anion.
我们研究了半胱氨酸衍生物福多司坦对气道炎症引起的气管微血管血流增加的影响。通过用二氧化硫（SO2）暴露 2 周的方法在兔子中引发气道炎症。每种药物（500mg/kg，po）或 0.5%羧甲基纤维素-Na（对照组）在 SO2 暴露前每天给药一次。最后一次 SO2 暴露结束后，通过血液灌注监测仪测量气管微血管的血流。福多司坦或 S-羧甲基半胱氨酸（S-CMC）显著抑制了 SO2 暴露引起的气管微血管血流增加。然而，福多司坦对 SO2 暴露兔子气管的药理学微血管反应没有影响。另一方面，福多司坦或 S-CMC 清除了来自大鼠中性粒细胞和黄嘌呤氧化酶-乙醛反应中酶促产生的超氧阴离子。结果表明，福多司坦抑制气管血流增加的作用至少部分是通过清除超氧阴离子来实现的，这与抗炎活性有关。
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