Spranger M, Kiprianova I, Krempien S, Schwab S
Department of Neurology, University of Heidelberg, Germany.
J Cereb Blood Flow Metab. 1998 Jun;18(6):670-4. doi: 10.1097/00004647-199806000-00009.
Respiratory burst activity of murine microglial cells was investigated in vitro under normoxic and hypoxic conditions with a chemoluminometric assay. Hypoxia for 24 hours reduced the release of extracellular reactive oxygen intermediates (ROIs), whereas reoxygenation increased the chemoluminescence more than sevenfold. Blockade of potassium channels inhibited the increase of oxidative burst after reoxygenation, indicating that potassium ions, which were increased in the supernatant of hypoxic microglial cells, were involved in this activation process. Also, blockade of voltage-gated calcium channels with nifedipine attenuated the increased release of ROIs. With fura-2 analysis, it was shown that the activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase by potassium ions was mediated by calcium influx via voltage-gated calcium channels. Thus, influx of calcium ions through voltage-gated channels activates the NADPH oxidase in microglial cells during reoxygenation. By the increased production of ROIs, microglial cells may add to the reperfusion injury after ischemia in vivo.
在常氧和低氧条件下，通过化学发光测定法体外研究了小鼠小胶质细胞的呼吸爆发活性。24小时的低氧状态降低了细胞外活性氧中间体（ROIs）的释放，而复氧后化学发光增加了七倍以上。钾通道的阻断抑制了复氧后氧化爆发的增加，这表明低氧小胶质细胞上清液中增加的钾离子参与了这一激活过程。此外，用硝苯地平阻断电压门控钙通道可减弱ROIs释放的增加。通过fura-2分析表明，钾离子对烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶的激活是由电压门控钙通道介导的钙离子内流所介导的。因此，在复氧过程中，通过电压门控通道的钙离子内流激活了小胶质细胞中的NADPH氧化酶。通过增加ROIs的产生，小胶质细胞可能会加重体内缺血后的再灌注损伤。
