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目的 :测定异丙酚对中性粒细胞 (PMN)激活后活性氧生成以及细胞内游离Ca2 + 浓度 ([Ca2 + ]i)的影响 ,探讨异丙酚影响PMN呼吸爆发的内在机制。方法 :利用电子自旋共振 (ESR)技术和自旋捕捉法 ,观察异丙酚对PMN呼吸爆发产生氧自由基 (ROS)的抑制作用 ;同时采用钙荧光指示剂 (Fura 2 /AM)负载离体PMN并行双波长模式测定不同浓度异丙酚对静息和激活状态下PMN细胞内 [Ca2 + ]i 的影响。结果 :高浓度 (75 μM)异丙酚可使静息状态下PMN细胞内 [Ca2 + ]i升高 ;在有钙基质中 ,异丙酚对趋化三肽 (fMLP)诱发的PMN胞内 [Ca2 + ]i 的升高有明显的降调作用 ,而在无钙基质中则不明显。在无钙基质中 ,高浓度 (≥ 5 0 μM )的异丙酚对fMLP诱发PMN呼吸爆发产生ROS有明显的抑制作用 ;而存在胞外钙浓度时 ,2 5 μM异丙酚的抑制程度更为明显。结论 :异丙酚可通过作用于胞外钙内流和胞内储存钙释放影响静息及激活状态下PMN胞内 [Ca2 + ]i;异丙酚在有钙基质中对PMN呼吸爆发产生ROS的抑制作用更为明显 ,提示异丙酚影响PMN胞内 [Ca2 + ]i,特别是对胞外钙内流的抑制作用 ,可能是其抑制PMN呼吸爆发的内在机制之一。
OBJECTIVE: To determine the effect of propofol on reactive oxygen species (ROS) production and intracellular free Ca2 + concentration ([Ca2 +] i) after activation of neutrophils (PMNs) and to explore the underlying mechanism of propofol on PMN respiratory burst. Methods: The inhibitory effect of propofol on the production of oxygen free radicals (ROS) from respiratory burst was observed by electron spin resonance (ESR) and spin catching method. Fura 2 / AM The effects of different concentrations of propofol on [Ca2 +] i in PMN cells under resting and activated state were measured by parallel PMN parallel dual wavelength mode. RESULTS: Propofol at high concentrations (75 μM) increased [Ca2 +] i in resting PMN cells; in the presence of calcium, propofol did not respond to chemotactic tripeptide (fMLP) -induced intracellular PMN [Ca2 +] i increased significantly lower role, but not in calcium-free matrix is not obvious. In calcium-free media, propofol at a high concentration (≥50 μM) significantly inhibited the ROS production induced by fMLP-induced respiratory burst in PMNs; whereas at extracellular calcium concentrations, propofol at 25 μM was more attenuated Obvious. CONCLUSIONS: Propofol can affect intracellular [Ca2 +] i in PMN at rest and in active state through the action of extracellular Ca2 + influx and intracellular Ca2 + release. Propofol produces ROS in respiratory burst of PMN in calcium matrix , Suggesting that propofol may affect the [Ca2 +] i in PMN, especially the inhibition of extracellular calcium influx, which may be one of the mechanisms underlying the prophylaxis of respiratory burst in PMN.