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歧化酶（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（l-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），1－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。
To investignte the changes of glutamate trareporter function, superoxide dismutase (SOD) achvity andmalondiadehyde (MDA) content in rats with injury of cerebral ischemia-reperfusion and antagonistical effect of dexanetha-sone. METHODS: A model of brain ischemia-reperfusion injury was estahlished by clipped three arteries and then releasedto repedese blood into brain in rats. The glutamte transporter funtions, SOD activities and MDA contents in cerebral con-tex, hippocampus and striatum of control, I-R and dexamethasone groups were detendned. RESULTS: Glutamate trans-porter function and SOD activity of ahave three sites in I-R group were decreased significanily (P < 0.05, P < 0.01 ) andMDA contents were incamd (P< 0.05, P < 0.01 ), comatal with control group. The glutamate transporter function,SOD achvity and MDA content in the ahave tae sites of I-R+dexamthasone group were recovered, compared with I-Rgroup. CONCLUSION: Oxygrn free radicals, which wele pnduced in the ischenda-repefuosion injury might result in theinhibihon of glutamate transporter. Dexamathasoe may antagonize the injury effect of the oxygen free radicals by acting onglutamate transporter in membrane.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1999年第10期865-867,共3页
Chinese Journal of Pathophysiology
基金
国家自然科学基金!39400051
关键词
脑缺血
再灌注损伤
地塞米松
谷氨酸转运体
Cerebral ischemia
Reperfusion injury
Free radicals
Dexamethasone
Rats
