葛根素治疗急性脊髓损伤机制的实验研究  

Mechanism Study of Puerarin Treatment for Acute Spinal Cord Injury

作　　者：田峰[1] 王斌[1] 季相禄[1] 田立杰[1] 

机构地区：[1]中国医科大学附属盛京医院骨外科,沈阳110004

出　　处：《中国医科大学学报》2013年第12期1126-1129,1136,共5页Journal of China Medical University

基　　金：辽宁省社会发展攻关计划(2012225081)

摘　　要：目的探讨葛根素治疗急性脊髓缺血再灌注损伤(SCI/RI)大鼠的机制。方法以雄性Sprague-Dawley大鼠建立SCI/RI模型,分别于再灌注1、2、4、6 h后以葛根素50 mg/kg进行腹腔内注射,然后每24 h注射相同剂量,持续2d。对谷氨酸水平、代谢型谷氨酸受体(mGluR)mRNA的表达以及细胞凋亡指数进行检查。再灌注后48 h时进行神经功能评估结果脊髓缺血再灌注损伤引起广泛的运动缺陷,这与谷氨酸水平和亲代谢型谷氨酸-1 mRNA表达水平升高相关,而葛根素抵制运动缺陷的进展,并降低谷氨酸水平,抑制亲代谢型谷氨酸-1 mRNA的表达。结论葛根素具有降低脊髓缺血/再灌注损伤的功能,葛根素的神经保护机制涉及减少谷氨酸释放量和降低亲代谢型谷氨酸-1Objective To explore the mechanism ofpuerarin treatment for acute spinal cord ischemia-reperfusion injury （SCI/RI） in rats. Meth- ods SCI/RI model was conducted in male Sprague-Dawley rots, and 50 mg/kg of puerarin was injected intraperitoneally at 1,2,4 and 6 h after re- peffusion, followed by same dose of injection every 24 h for 2 days. Glutamate level, metabotropic glutamate receptors （mGluR）, mRNA expression, and apoptosis indices were determined. Neurologic function was assessed at 48 h after repeffusion. Results SCI/RI caused extensive motor deficit associated with an elevation of glutamate level and increased mGhiRs- 1 mRNA expression, while puerarin administration improved motor deficit, re- duced glutamate level, and inhibited mGluRs- 1 mRNA expression. Conclusion The present study demonstrated that administration of puerarin re- duced the spinal ischemia/reperfusion injury, and the results indicated a decrease in glutamate release and mGluRs- 1 mRNA expression may be in- volved in neuropmtective mechanism of puerarin.

关 键 词：葛根素 脊髓缺血再灌注 代谢型谷氨酸受体 谷氨酸 凋亡 

分 类 号：R653.2[医药卫生—外科学]