川芎嗪促进脑缺血耐受形成的作用及机制研究  

Research on Effect of Ligustrazine on Promoting Ischemia Tolerance Formation

作　　者：胡永红[1,2] 周爱民[1,2] 田野[1,2] 朱钰宝[1,2] 

机构地区：[1]石家庄市中医院 [2]河北医科大学,河北石家庄050051

出　　处：《中国中医基础医学杂志》2010年第8期671-674,共4页JOURNAL OF BASIC CHINESE MEDICINE

摘　　要：目的:通过动物实验证实川芎嗪(tetramethylpyrazine,TMP)具有增强CIP(脑预缺血,cerebral ischemicpreconditioning)脑保护效果,促进脑缺血耐受形成的作用。方法:将96只健康昆明小鼠随机分为假手术组、缺血损伤组、BIT模型组、TMP干预组4组,采用生化方法检测脑组织NOS活性和NO含量;采用免疫组化方法检测海马组织Bax和bcl-2蛋白表达。HE染色,光镜下观察海马CA1区组织学分级和神经元密度(neuronal density,ND)。结果:缺血损伤组小鼠脑组织NOS活性(51.72±7.07U/gprot)、NO含量(1.78±0.21μmol/gprot)和BIT模型组NOS活性(50.45±6.18 U/gprot)、NO含量(1.69±0.12μmol/gprot)与假手术组NOS活性(17.01±4.96 U/gprot)和NO含量(0.71±0.14μmol/gprot)相比明显升高(P<0.01),但两者之间无差别。TMP干预组NOS活性(34.74±4.18U/gprot)、NO含量(1.33±0.11μmol/gprot)较缺血组、BIT模型组明显降低(P<0.01),而较假手术组又明显升高(P<0.01)。与假手术组相比,缺血损伤组、BIT模型组Bax、bcl-2表达明显增多(P<0.01),而两者之间无差异。TMP干预组较缺血损伤组、BIT模型组Bax表达明显减弱(P<0.05),bcl-2表达明显增强(P<0.05)。而较假手术组Bax、bcl-2表达明显增强(P<0.01)。结论:在CIP诱导BIT形成过程中,通过川芎嗪的干预,能够使缺血脑组织NOS活性下降,NO含量降低,bcl-2蛋白表达增多,Bax蛋白表达减少,这可能是其提高CIP脑保护效果、增强脑缺血耐受的重要机制之一。Objective： Animal experiments confirmed that TMP（tetramethylpyrazine,TMP） with enhanced CIP（cerebral ischemic preconditioning,cerebral ischemic preconditioning） effect of brain protection,promote the role of the formation of brain ischemic tolerance.Methods： 96 healthy Kunming mice were randomly divided into four groups： sham operation group,ischemia injury group,BIT model group,TMP intervention group,using biochemical methods detect brain tissue NOS activity and NO content;detected by immunohistochemistry hippocampus Bax and bcl-2 protein expression.HE staining,light microscopy observation of histological grade in hippocampal CA1 area and neuron density（neuronal density,ND）.Results： The ischemic injury in mice brain tissue NOS activity（51.72 ± 7.07U/gprot）,NO levels（1.78 ± 0.21μmol/gprot） and the BIT model group,NOS activity（50.45 ± 6.18 U/gprot）,NO content（1.69 ± 0.12μmol/ gprot） and NOS activity in sham-operated group（17.01 ± 4.96 U/gprot） and NO levels（0.71 ± 0.14μmol/gprot） significantly higher than（P〈0.01）,but no difference between the two.NOS activity of TMP in the intervention group（34.74 ±4.18 U/gprot）,NO levels（1.33 ± 0.11μmol/gprot） compared with ischemic group,BIT model group was significantly lower（P〈0.01）,and compared with the sham group was significantly higher（P〈0.01）.Compared with the sham-operated group,ischemia injury group,BIT model group,Bax,bcl-2 expression was significantly increased（P〈0.01）,whereas no difference between the two.TMP in the intervention group compared with ischemic injury group,BIT model group,Bax expression was significantly reduced（P〈0.05）,bcl-2 expression was significantly increased（P〈0.05）.Compared with the sham operation group,while Bax,bcl-2 expression was significantly increased（P〈0.01）.Conclusion： BIT-induced formation of CIP,through the intervention of TMP,enabling ischemic brain tissue decreased NOS activity,NO content decreased,bcl-2 protein expression incre

关 键 词：脑预缺血 小鼠 NO NOS BAX 

分 类 号：R285.5[医药卫生—中药学]