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作 者:房雷[1] 王岭[1] 孙丽[1] 孙锋[1] 王超[1]
机构地区:[1]青岛大学医学院第二附属医院神经内科,中国青岛266100
出 处:《国际老年医学杂志》2011年第4期150-153,共4页International Journal of Geriatrics
摘 要:目的:探讨胡黄连苷Ⅱ在大鼠脑缺血再灌注损伤中的抗氧化作用。方法:成龄健康Wistar大鼠100只,应用线栓法建立MCAO/R模型,经尾静脉注射胡黄连苷Ⅱ10mg/kg。Bederson’s法进行神经功能评分,氯化三苯基四氮唑(TTC)染色法测定脑梗死体积,TUNEL法检测细胞凋亡,酶联免疫吸附试验(ELISA)检测脑组织匀浆中诱生型氧化氮合酶(iNOS)和超氧化物歧化酶(SOD)的含量。结果:胡黄连苷Ⅱ组神经行为功能、脑梗死体积低于模型对照组(P〈0.05);脑组织匀浆iNOS和TUNEL阳性细胞数量均低于模型对照组(P〈0.05);而脑组织匀浆SOD均高于模型对照组(P〈0.05)。结论:胡黄连苷Ⅱ可能通过下调iNOS表达和上调SOD表达来抑制细胞凋亡,有一定的保护作用。OBJECTIVE: To explore the antioxidant effects of picroside Ⅱ on the cerebral ischemia reperfusion injury in rats. METHODS : The MCAO/R model was established with a suture blocking in the MCA of 100 ripe healthy Wistar rats and treated by injecting picroside Ⅱ(10mg/kg) from the tail vein. The nervous behavioral function was evaluated with Bederson' s test. The cerebral infarction volume was observed with tetrazolium chloride (TFC) staining. The concentration of indueibale nitic oxide synthse (iNOS) and superoxide dismutase (SOD) in brain tissue was determined by ELISA. TUNEL positive cells were counted by immunofluoresence assay. RESULTS: In picroside Ⅱ group rats, the nevous behavioral malfunction, the cerebral infarction volume, the concentration of iNOS and the number of TUNEL positive cells were significantly lower than those in model control group ( P 〈 0. 05 ) , while the coneentration of SOD was extremely higher than that in model control group (P 〈 0. 05 ). CONCLUSION : Pieroside Ⅱ might play a neuroprotective effect by reducing expressions of iNOS and enhancing expressions of SOD to inhibit neuronal apoptosis in cerebral isehemie in rats.
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