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作 者:李冬利[1] 于洪儒[1] 杨菁[1] 王洪新[1] 梁巍巍[1] 张挺[1]
出 处:《中国新药杂志》2006年第14期1169-1172,共4页Chinese Journal of New Drugs
摘 要:目的:观察牛血活性肤(BAPE)对缺氧损伤心肌细胞的影响,并探讨其作用机制。方法:用Na_2S_2O_4法建立心肌细胞缺氧损伤模型,以培养液中乳酸脱氢酶(LDH)活性、细胞内线粒体脱氢酶活性和细胞存活率为指标,观察BAPE在0.004~1.5mg·mL^(-1)浓度对缺氧心肌的保护作用;同时观察BAPE在0.02~1.5mg·mL^(-1)浓度对正常心肌细胞D-[6-~3H]葡萄糖转运和线粒体脱氢酶活性的影响。结果:BAPE在浓度为0.004~1.5mg·mL^(-1)时能显著降低缺氧心肌细胞培养液的LDH活性,提高细胞存活率,增强缺氧心肌细胞线粒体脱氢酶活性,当浓度为0.5mg·mL^(-1)时作用最强(P<0.01),但当浓度达1.5mg·mL^(-1)时,作用受抑制(P<0.05);当BAPE浓度为0.1~0.5 mg·mL^(-1)时能促进正常心肌细胞对D-[6-~3H]葡萄糖的吸收和线粒体脱氢酶活性(P<0.05)。结论:BAPE对缺氧损伤心肌细胞具有保护作用,其机制可能与提高细胞对葡萄糖的摄取和利用,增强细胞内的线粒体脱氢酶活性有关。Objective: To study the protection and mechanism of calf blood active peptide extract (BAPE) on hypoxic myocardium. Methods: A model of hypoxic myocardium was established by culturing of Na2S2O4 with calf myocardial tissues. The protective effects of the myocardial tissues from the hypoxic injury by BAPE 0. 004 - 1.5mg·mL^-1 were assessed based on status of lactic dehydrogenase (1,DH) levels in cuhure media, the cellular survival rate and the dehydrogenase levels in the myocardial mitochondria. The D-[ 6-3H ] glucose uptake and mitoehondria dehydrogenase levels of healthy myocardial cells were measured in the existence of BAPE 0.02 - 1.5 mg·mL^-1. Result: BAPE significantly reduced LDH levels in the hypoxic myocytes and increased the cellular survival rate and the activities of mitochondria dehydrogenase in a dose-dependent setting. The most potent effects of BAPE were observed at the concentration of 0. 5mg·mL^-1(P 〈0. 01) and the inhibition was found at the concentration of 1.5mg·mL^-1(P 〈0.05). BAPE significantly improved the glucose uptake and mitochondria dehydrogenase levels in the healthy myocardial cells in the concentration of BAPE 0. 1~0.5 mg·mL^-1 ( P 〈 0.05 ). Conclusion : BAPE protected the myocardial cells from hypoxic injury by improving the glucose uptake and the activities of mitochondria dehydrogenase.
关 键 词:牛血活性肽 缺氧 心肌保护 线粒体脱氢酶 葡萄糖
分 类 号:R845.22[医药卫生—航空、航天与航海医学] R965.1[医药卫生—临床医学]
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