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大鼠脑缺血 |
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任晓燕 曲忠森 葛宝林 张玉敏 徐珞
摘要 目的：探讨大鼠脑缺血-再灌注损伤时脑组织谷氨酸转运体功能及超氧化物岐化酶(SOD)活性、脂质过氧化物丙二醛(MDA)含量变化及地塞米松对其的影响。方法：采用大鼠三血管夹闭、松夹制作大鼠完全性脑缺血-再灌注损伤的模型。测定假手术对照组、脑缺血-再灌注损伤(I-R)组和I-R+地塞米松组的皮层、海马、纹状体的谷氨酸转运体功能及SOD活性、MDA含量的变化。结果：脑缺血-再灌注损伤时3个部位的谷氨酸转运体的功能均明显降低(P＜0.05，P＜0.01)、SOD活性显著降低(P＜0.05，P＜0.01)，MDA含量明显升高(P＜0.05，P＜0.01)，I-R+地塞米松组的3部位谷氨酸转运体功能与I-R组相比有明显恢复(P＜0.05，P＜0.01)，与对照组已无明显差异(P＞0.05)；SOD活性回升(P＜0.05，P＜0.01)、MDA含量回降(P均＜0.05)。结论：大鼠脑缺血-再灌注损伤时脑组织三部位的谷氨酸转运体功能降低，且可能与自由基效应有关；而地塞米松则可能通过抗自由基效应使谷氨酸转运体功能恢复而发挥其抗损伤作用。
主题词 脑缺血；再灌注损伤；自由基；地塞米松；大鼠
Damage of glutamate transporter function during ischemia-reperfusion
injury of rat brain and antagonistical effect of dexamethasone
REN Xiao-Yan,QU Zhong-Sen,GE Bao-Lin,ZHANG Yu-Min,XU Luo
Qingdao University Medical College,Qingdao(266021)
Abstract AIM:To investigate the changes of glutamate transporter function,superoxide dismutase (SOD) activity and malondiadehyde (MDA) content in rats with injury of cerebral ischemia-reperfusion and antagonistical effect of dexamethasone.METHODS：A model of brain ischemia-reperfusion injury was established by clipped three arteries and then released to reperfuse blood into brain in rats.The glutamate transporter functions,SOD activities and MDA contents in cerebral contex,hippocampus and striatum of control,I-R and dexamethasone groups were determined.RESULTS：Glutamate transporter function and SOD activity of above three sites in I-R group were decreased significantly (P＜0.05，P＜0.01) and MDA contents were increased (P＜0.05，P＜0.01),compared with control group.The glutamate transporter function,SOD activity and MDA content in the above three sites of I-R+dexamethasone group were recovered,compared with I-R group.CONCLUSION：Oxygen free radicals,which were produced in the ischemia-reperfusion injury might result in the inhibition of glutamate transporter.Dexamathasone may antagonize the injury effect of the oxygen free radicals by acting on g[1] [2] 下一页
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