夏天无总碱抗实验性脑缺血的作用  

Effects of Corydalis ambailis migo total alkaloids on experimental cerebral ischemia

作　　者：胡雪勇 孙安盛[2] 余丽梅[2] 吴芹[2] 

机构地区：[1]南昌铁路中心医院药剂科,江西南昌330003 [2]遵义医学院药理学教研室,贵州遵义563003

出　　处：《中西医结合学报》2005年第1期46-49,共4页Journal of Chinese Integrative Medicine

基　　金：贵州省自然科学基金资助项目 (No .2 0 0 0 30 4 0 )

摘　　要：目的 :观察夏天无总碱 (Corydalisambailismigototalalkaloids ,COAMTA)对脑缺血 /再灌注损伤的保护作用并对其机制作初步探讨。方法 :采用小鼠断头张口喘气模型、大鼠大脑中动脉缺血 2h/再灌注2 2h模型 ,以神经病学评分、脑梗死范围及脑组织水含量变化 ,观察COAMTA抗脑缺血 /再灌注损伤的效应 ;通过测定大鼠脑组织中一氧化氮合酶 (nitricoxidesynthase ,NOS)、超氧化物歧化酶 (superoxidedismutase ,SOD)活性及丙二醛 (malondialdehyde ,MDA)含量的变化 ,并采用原位末端标记法观察对神经细胞凋亡的影响以探讨药物作用的机制。结果 :COAMTA可延长小鼠张口喘气时间 ,降低大鼠脑缺血 /再灌注后神经病学评分及梗死范围 ,降低脑组织MDA含量和NOS活性及升高SOD活性 ,COAMTA还可抑制神经细胞凋亡。结论 :COAMTA对脑缺血 /再灌注损伤有保护作用 ,其作用机制与抑制NOS活性、提高SOD活性、减少神经细胞脂质过氧化损伤和抑制神经细胞凋亡有关。Objective： To observe the protective effects of Corydalis ambailis migo total alkaloids（COAMTA） on cerebral ischemia/reperfusion injury in rats and to investigate its mechanism. Methods： The effects of COAMTA on decapitated gasping mouse model and rat model of middle cerebral artery ischemia （2 h）/reperfusion （22 h） were observed. The neurological scale, cerebral infarcted volume and cerebral water content subjected to cerebral middle artery ischemia/reperfusion in rats were recorded. The activities of nitric oxide synthase （NOS） and superoxide dismutase （SOD） and the content of malondialdehyde （MDA）in the rats＇ brain were measured. Cell apoptosis in ischemic penumbral area was observed with light microscope in the method of terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling （TUNEL）. Results： The average gasping time of the mice （6. 0 mg/kg or 9. 0 mg/kg COAMTA） was significantly prolonged, the cerebral infarcted volume and cerebral water content of the rats （5.0 mg/kg or 7.5 mg/kg COAMTA） were significantly decreased, as compared with the control groups. The average activity of SOD in cerebral tissue of the rats （5.0 mg/kg or 7.5 mg/kg COAMTA） was significantly higher than that of the control groups, meanwhile, the average activity of NOS and the content of MDA declined significantly. The cell apoptosis in ischemic penumbral area of the rats （5.0 mg/kg COAMTA） was significantly inhibited as compared with the control groups. Conclusion： COAMTA can facilitate the protection against cerebral ischemia/reperfusion damage. The mechanism is related to inhibiting the activity of NOS and lipoperoxidation, increasing the activity of SOD and decreasing the neuronal apoptosis.

关 键 词：夏天无 脑缺血 神经病学表现 一氧化氮合酶 超氧化物歧化酶 丙二醛 

分 类 号：R743.3[医药卫生—神经病学与精神病学]