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目的 :探讨 NO在外源性自由基损伤内皮细胞 (EC)中的作用。方法 :培养的家兔主动脉 EC随机分为四组 :1.对照组 (C,n=6 ) :2 ml PBS;2 .自由基损伤组 (X/XO,n=6 ) :2 m l PBS中加入终浓度为 1μm ol/ml X,0 .1IU/ml的XO;3.L - Arg组 :含终浓度为 10 - 3M的 L - Arg,余同 2 ;4.SNP组 :含终浓度为 10 - 5 M的 SNP,余同 2。在观察 L- NAME对自由基损伤的作用时 ,在缓冲液中加入终浓度为 10 - 4 M的 L- NAME,余同 2。四组细胞置于 37℃、5 % CO2 孵箱中孵育 2小时后 ,测定乳酸脱氢酶 (L DH)、丙二醛 (MDA)含量及血管紧张素转换酶 (ACE)活性。结果 :1μmol/m l的 X和 0 .1IU/ml XO可引起 EC的 L DH、MDA含量明显增加 ,10 - 3Μ的 L - Arg及 10 - 5 M的 SNP,均可减轻自由基对EC的损伤 ,10 - 4 M的 L- NAME则可加剧外源性自由基对 EC的损伤
Objective: To investigate the role of nitric oxide in endothelial cells (ECs) induced by exogenous free radicals. Methods: The cultured aorta of rabbits were randomly divided into four groups: 1. Control group (C, n = 6): 2 ml PBS; 2. Radical injury group (X / XO, n = 6) Add XO at a final concentration of 1μmol / ml X and 0.1IU / ml; 3. L - Arg group: containing L - Arg at a final concentration of 10 - 3M, with the same 2; 4. SNP group: 10 - 5 M for the SNP, the same as 2. To observe the effect of L-NAME on free radical damage, L-NAME at a final concentration of 10 - 4 M was added to the buffer. Four groups of cells were incubated at 37 ℃ for 2 hours in 5% CO2 incubator. L DH, MDA and ACE activity were measured. Results: 1 μmol / ml X and 0.1 IU / ml XO induced a significant increase in L DH and MDA content of EC. Both 10 - 3 M L - Arg and 10 - 5 M SNP reduced the EC damage induced by free radicals , 10 -4 M L-NAME can exacerbate the damage of exogenous free radicals on EC