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【目的】了解实验性血瘀证动物模型血管内皮细胞中一氧化氮合酶 (NOS)的基因表达及其分泌NO的变化。【方法】用半定量RT -PCR方法检测模型组体内血管内皮细胞及体外培养的细胞中组成型一氧化氮合酶mRNA的表达 ,并相应测定分泌的NO水平。【结果】与对照组比较 ,模型组兔体内血管内皮细胞中组成型NOS (cNOS)基因表达以及血浆和原代培养液中NO水平皆明显下降 (P <0 .0 1) ,同期血浆中NO含量与内皮细胞中cNOSmRNA的表达水平呈正相关 (r=0 .739,P <0 .0 1)。两组间体外培养的传代细胞中cNOS基因表达及培养液上清中NO含量无明显差异 (P >0 .0 5) ,但NO水平都比各自原代培养液中的明显升高 (P <0 .0 1,P <0 .0 5)。【结论】短期内血瘀证兔模型体内内源性NO水平降低主要是cNOS基因表达下降导致的 ,随时间的延长 ,不排除诱导型NOS (iNOS)及体内其他因素对分泌NO的综合影响
【Objective】 To investigate the gene expression and secretion of nitric oxide synthase (NOS) in vascular endothelial cells of experimental rat model of blood stasis. 【Method】 The expression of constitutive nitric oxide synthase mRNA in vascular endothelial cells and cultured cells in vitro and in vivo were detected by semi-quantitative RT-PCR. The level of NO secretion was measured accordingly. 【Results】 Compared with the control group, the expression of cNOS gene and the levels of NO in plasma and primary culture medium were significantly decreased in the model group (P <0.01), while NO The content of cNOS mRNA was positively correlated with the level of cNOS mRNA in endothelial cells (r = 0.73, P <0.01). There was no significant difference in the expression of cNOS gene and the content of NO in the supernatant between the two groups (P> 0.05), but the level of NO was higher than that in the original culture medium (P < 0 .0 1, P <0. 0 5). 【Conclusion】 The decrease of endogenous NO levels in blood stasis syndrome rabbits in short term is mainly caused by the decrease of cNOS gene expression. With the prolongation of time, the combined effects of inducible NOS (iNOS) and other factors in vivo on the secretion of NO are not excluded