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本研究旨在探索在大鼠心肌梗死过程中内源性硫化氢(H2S)与一氧化氮(NO)对心肌组织的保护作用和两种气体分子之间的相互作用关系。将试验动物随机分成五组,分别给予H2S合成酶胱硫醚-γ-裂解酶(CSE)的抑制剂炔丙基甘氨酸(PAG)和CSE内源性底物左旋半胱氨酸(L-Cysteine),以及NO的合成酶(eNOS)的抑制剂L-NAME和激活剂西地那非(sildenafil),同时设置生理盐水组为对照。给药第七天,建立大鼠心肌梗死动物模型, 存活大鼠继续观察48小时。通过对五组试验动物死亡率和心肌梗死面积,血浆中NO和H2S的水平,以及心肌组织中CSE酶的活性和CSE和eNOS蛋白水平表达改变和基因水平mRNA的表达变化综合分析,我们认为内源性H2S和NO对大鼠心肌梗死均有保护作用,H2S-CSE体系和 NO-eNOS体系在大鼠心肌梗死过程中呈相互下调的关系趋势。
This study aimed to explore the protective effect of endogenous hydrogen sulfide (H2S) and nitric oxide (NO) on myocardial tissue and the interaction between two gas molecules during myocardial infarction in rats. The experimental animals were randomly divided into five groups and were given propargylglycine (PAG), an inhibitor of H2S synthase cystathionine-γ-lyase (CSE), and L-Cysteine ) As well as L-NAME, an inhibitor of NO synthase (eNOS), and sildenafil, an activator, were set as controls. On the seventh day after administration, an animal model of myocardial infarction in rats was established and survived rats were observed for 48 hours. Through the five groups of animal mortality and myocardial infarction area, the level of NO and H2S in plasma, as well as myocardial tissue activities of CSE enzyme and CSE and eNOS protein expression and gene expression level changes in a comprehensive analysis, we think within H2S and NO have protective effects on myocardial infarction in rats. H2S-CSE and NO-eNOS show a downward trend in myocardial infarction.