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作 者:王旭兰[1] 王群让 康平[3] 宋宝国[4] 常凤军[4]
机构地区:[1]咸阳职业技术学院医学院护理部,咸阳712000 [2]陕西中医药大学附属医院心内科 [3]延安大学附属医院东关医院心脑血管外科 [4]陕西省人民医院心脏外科
出 处:《山西医科大学学报》2015年第9期858-860,共3页Journal of Shanxi Medical University
基 金:陕西省科技计划基金资助项目(2012SF2-01)
摘 要:目的探讨左旋精氨酸(L-Arg)是否可以改善肺高压(PH)大鼠体内循环颗粒(MPs)对内皮型一氧化氮合酶(e NOS)的抑制作用,以进一步了解L-Arg防治肺动脉高压的机制。方法 SD雄性大鼠18只(n=6):对照组,野百合碱组(MCT组),L-Arg组。除对照组外,MCT组和L-Arg组大鼠腹腔注射野百合碱诱导PH模型并饲养3周;期间L-Arg组大鼠每日注射L-Arg,对照组和MCT组每日注射与L-Arg等量的生理盐水。3周时测大鼠肺动脉压力后取血提取MPs,然后检测各组MPs含量及各组MPs对大鼠肺血管内e NOS蛋白表达的影响。结果与对照组比较,MCT组和L-Arg组的MPs含量均升高(P<0.05),但L-Arg组较MCT组稍有下降(P<0.05);与对照组比较,MCT组和L-Arg组的e NOS蛋白表达均降低(P<0.001)。结论 L-Arg可以减少肺高压大鼠体内的MPs的含量,但并不能改善MPs对肺血管内e NOS蛋白的抑制作用,提示L-Arg改善PH的主要机制不是直接影响MPs功能实现的。Objective To investigate the effects of L-arginine(L-Arg) on circulating microparticles(MPs) inhibiting endothelial nitric oxide synthase(eNOS) in rats with pulmonary hypertension (PH), and to explore its preventive mechanism for pulmonary hyperten- sion. Methods Eighteen SD male rats were randomly divided into three groups: control group, MCT group and L-Arg group. The rats in MCT group and L-Arg group were intraperitoneally injected with monocrotaline (MCT) to induce PH model and bred for 3 weeks. During the 3 weeks, the rats were daily injected with L-Arg in L-Arg group, and the same amount of saline in control group and MCT group. At 3 week after modeling, the pulmonary artery pressure was measured, and the levels of MPs and the expression of eNOS protein in rat pulmonary artery were examined. Results Compared with control group, MPs content were increased in MCT group and L-Arg group, but MPs in L-Arg group decreased slightly compared with MCT group( P 〈 0.05 ). Compared with control group, the ex- pression of eNOS in both MCT group and L-Arg group were downregulated, but the eNOS expression showed no significant difference between MCT group and L-Arg group( P 〈 0. 001 ). Conclusion L-Arg can reduce the level of MPs in rats with pulmonary hyperten- sion, but can not block the inhibitive effects of microparticles on eNOS protein expression, which suggests that the effects of L-Arg on PH may not be caused mainly through MPs pathway.
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