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Protective effect of penehyclidine hydrochloride in cerebral ischemia-reperfusion injury rats
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- Author:
- No author available
- Journal Title:
- CHINESE JOURNAL OF EMERGENCY MEDICINE
- Issue:
- 9
- DOI:
- 10.3760/j.issn:1671-0282.2007.09.009
- Key Word:
- 盐酸戊乙奎醚;脑缺血-再灌流损伤;细胞凋亡;Bcl-2;Bax;大鼠
Abstract： 目的 探讨盐酸戊乙奎醚对大鼠三动脉阻断法急性全脑缺血-再灌流损伤的保护作用.方法 144只雄性SD大鼠随机分为假手术组、缺血-再灌流组(生理盐水1 ml)、东莨菪碱组(0.01mg/kg)和盐酸戊乙奎醚组(0.01 mg/kg),缺血前40 min分别腹腔注射相应药物,缺血时间为10min,于再灌流24 h、3 d和7 d测定其行为学(开阔法、平衡木法、攀绳和肌力试验),再灌流2 h、12 h、24 h、3 d和7 d取材测定海马CA1区存活神经元数量(HE染色)、凋亡神经元数量(TUNEL染色)、bcl-2和bax蛋白表达(免疫组化染色),部分大鼠于再灌流4 d测定脑梗死体积(TTC法).结果 与缺血-再灌流组比较,盐酸戊乙奎醚组和东莨菪碱组海马CA1区凋亡神经元数量减少(P＜0.01),bcl-2提前并延长表达(P＜0.01),盐酸戊乙奎醚组bax表达下降(P＜0.05或P＜0.01).同时,盐酸戊乙奎醚组和东莨菪碱组存活神经元数量增加(P＜0.05),脑梗死体积缩小(P＜0.05或P＜0.01),行为学检测指标改善(P＜0.05).盐酸戊乙奎醚组较东莨菪碱组作用更加明显(P＜0.05).结论 盐酸戊乙奎醚对脑缺血-再灌流损伤大鼠具有脑保护作用,并且优于同样剂量东莨菪碱.改变bcl-2/bax的比例可能是其机制之一.
- [1]韩继媛,曹锋生,王一镗,等.长托宁的临床应用[J].2005,(2).
- [2]叶心国,余绍祖,李承晏.亚低温对大鼠缺血-再灌流后脑梗死体积、神经功能及炎症反应的影响[J].2006,(6).
- [3]李昂,段美丽,翁以炳,等.盐酸戊乙奎醚（长托宁）治疗脓毒性休克的临床研究[J].2006,(8).
- [4]李文迅,韩焱晶,陶娟,等.电针对抑郁模型大鼠海马神经元凋亡的影响[J].2005,(2).
- [5]高谦,吴宗耀,姚志彬.运动训练促进小鼠脑局灶缺血后功能恢复[J].2000,(5).
- [6]Mark P. Mattson.Acetylcholine potentiates glutamate-induced neurodegeneration in cultured hippocampal neurons[J].1989,497(2).
- [7]关新民主编.医学神经生物学纲要[M].2003.
- [8]DM Feeney,A Gonzalez,WA Law.Amphetamine, haloperidol, and experience interact to affect rate of recovery after motor cortex injury[J].1982,217 (4562).
- [9]Fukuda K,Uchimura H,Takasawa R,etc.DNA fragmentation in ischemic core and penumbra in focal cerebral ischemia in rats.[J].2001,91(1).
- [10]Jagannathan NR,Gupta YK,Briyal S,etc.Effect of endothelin antagonist (TAK-044) on cerebral ischemic volume, oxidative stress markers and neurobehavioral parameters in the middle cerebral artery occlusion model of stroke in rats.[J].2005,77(1).
- [11]Kameyama M.,Suzuki J.,Shirane R.,etc.A new model of bilateral hemispheric ischemia in the rat--three vessel occlusion model[J].1985.
- [12]Cheng D,Sapolsky RM,Steinberg GK,etc.Bcl-2 overexpression protects against neuron loss within the ischemic margin following experimental stroke and inhibits cytochrome c translocation and caspase-3 activity.[J].2003,85(4).