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作 者:周鹏[1] 何昱[1] 杨洁红 张宇燕[1] 周惠芬[1] 赵涛 付巍 万海同[1]
机构地区:[1]浙江中医药大学心脑血管病研究所,浙江杭州310053 [2]山东步长制药股份有限公司,山东菏泽274000
出 处:《中国中药杂志》2014年第24期4844-4848,共5页China Journal of Chinese Materia Medica
基 金:国家自然科学基金项目(81173647;81373898;81274176;81473587);浙江省自然科学基金项目(LR12H27001)
摘 要:为研究丹红注射液对缺氧损伤脑微血管内皮细胞(r BMECs)的保护机制。该实验采用原代培养乳鼠脑微血管内皮细胞并进行Ⅷ因子鉴定,建立缺氧4 h损伤模型的同时,丹红注射液(25,50,100 m L·L-1)作用于r BMECs,生化法检测细胞中超氧化物歧化酶(SOD)活性和丙二醛(MDA)水平,RT-PCR法检测细胞MMP-9,ICAM-1,P53 mRNA表达水平,透射电镜观察细胞超显微结构变化。结果表明缺氧使原代培养的r BMECs受到明显损伤,与模型组比较,丹红注射液(50,100 m L·L-1)可显著对抗缺氧造成的损伤,增强SOD活性,降低MDA水平,明显下调MMP-9,ICAM-1,P53 mRNA的表达,丹红注射液100 m L·L-1能够保护细胞正常的形态、显微结构、维持细胞间紧密连接,抑制缺氧诱导的细胞凋亡。从结果中可以得出丹红注射液对缺氧损伤r BMECs具有明显的保护作用,其机制与增强细胞抗氧化能力,抑制炎症反应及细胞凋亡有关。To study the protective mechanism of Danhong injection on brain microvascular endothelial ceils (rBMECs) injured by hypoxic. In the experiment, primary suckling mouse's rBMECs cells were collected and identified with factor Ⅷ to establish the 4 h injury model. Meanwhile, rBMECs were given Danhong injection (25, 50, 100 mL · L^-1), and the superoxide dismutase (SOD) activity and the malonyldialdehyde (MDA) level were detected by the biochemical method. Cell MMP-9, ICAM-1 and P53 mRNA expression levels were detected by RT-PCR method. Changes in cells' microscopic structure were observed by transmission electron microscope. According to the results, primary rBMECs were notably injured by hypoxia. Compared with model group, Danhong injection (50, 100 mL ·L^-1) could remarkably resist the injury induced by hypoxic, increase intracellular SOD activity, decrease MDA level and significantly down-regulate ICAM-1, MMP-9 and 1953 mRNA expressions. Danhong injection ( 100 mL ·L^-1 ) could protect the cells' normal morphology and microscopic structure, maintain the close intercellular junction, and inhibit the hypoxia-induced cell apoptosis. The results showed that Danhong injection plays a significant role in protecting rBMECs injured by hypoxia. Its mechanism may be related to the enhancement of cells' antioxidant capacity, the inhibition of inflammatory resoonse and the cell apoptosis.
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