The roles and the kinetics of gp91 phox after traumatic brain injury in mice

脑创伤后超氧阴离子自由基(O2-)产生的来源有环氧合酶、黄嘌呤加氧酶、NADPH加氧酶等。本研究利用gp9lPhox基因敲除小鼠，研究了gp9lPhox(Gp91)在创伤性脑损伤后的动态变化及其作用。在本研究中，我们用Western blotting方法研究了小鼠创伤性脑损伤模型(对照皮质撞击模型)中gp9lPhox的表达随时间的变化。采用双重免疫组织化学技术对gp91阳性细胞进行鉴定。并于伤后第2天测量野生鼠和gp9lPhox基因敲除小鼠的损伤面积。结果伤后第2天，gp91Phox主要在小胶质细胞中强表达。在gp91Phox基因敲除小鼠中，损伤区域被抑制。在gp91Phox基因敲除小鼠中，超氧阴离子自由基的产生也受到抑制，提示gp91Phox和NADPH在脑损伤中起着重要的自由基产生作用。

(Introduction)The sources of superoxide radical (O2-) production following traumatic brain injury (TBI) are known as some cascades: cyclooxygenase, xanthine oxygenase, NADPH oxygenase. In this study, the kinetics and the roles of gp9lphox(gp91) after traumatic brain injury were investigated using gp9lphox gene knockout mouse.(Material and Methods)C57BL mice were used in this study. In the current study, we investigated the time-dependent changes in the expression of the gp9lphox in the mice traumatic brain injury model (TBI) (controlled cortical impact model) using western blotting method. The gp91 positive cells were identified by double immunohistochemical technique. The damaged areas of wild mouse and gp9lphox knockout mouse were also measured on day2 after TBI. Superoxide radical levels were detected by in situ detection of oxidized Het.(Results)On day 2 after TBI, the gp91 phox was strongly expressed in microglia mainly. The damaged area was suppressed in gp91 phox knockout mouse. Production of superoxide radical was also suppressed in gp91 phox knockout mouse.These results indicate that gp91phox and NADPH has the important roles as a generator of free radical in TBI.