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作 者:王青[1] 王桂芹[1] 庞玲霞[1] 薛峰[1] 陈醒言[1] 陈然[1] 孔晓霞[1] 龚永生[1] 范小芳[1]
机构地区:[1]温州医学院低氧医学研究所机能实验教学中心,浙江温州325035
出 处:《中国应用生理学杂志》2013年第2期101-105,I0001,共6页Chinese Journal of Applied Physiology
基 金:浙江省自然科学基金(Y2091033);高原医学教育部重点实验室(第三军医大学)资助项目(2011JSGY07)
摘 要:目的:探讨新的小分子活性肽apelin及其受体(APJ)在野百合碱诱导的肺动脉高压大鼠肺组织中的变化及意义。方法:雄性SD大鼠25只,随机分为对照组(n=10)和野百合碱组(n=15)。野百合碱组大鼠一次性腹部注射野百合碱60 mg/kg,对照组注射相同剂量的溶媒。注射野百合碱后第21天时,测定大鼠平均肺动脉压,HE染色观察肺组织病理学变化,Masson三色染色检测肺血管重建指标,放射免疫法及Western blot法测定肺组织中apelin和APJ的蛋白,RT-PCR法观察肺组织apelin和APJ的基因。结果:野百合碱组的平均肺动脉压、右心室肥大指数、肺血管重建指标、肺组织中apelin蛋白含量均明显高于对照组,而肺组织中APJ蛋白及基因表达显著低于对照组(P<0.05,P<0.01);但肺组织apelin基因表达两组间无显著统计学差别。免疫组化定位发现,野百合碱组大鼠apelin及APJ蛋白在肺组织内的炎症细胞胞膜及胞浆内呈强阳性表达。结论:内源性apelin及其受体的表达异常可能在野百合碱诱发的肺动脉高压的发生发展中起重要作用。Objective: To observe the change of apelin and its receptor (APJ) in the lung tissue of rats with pulmonary hypertension induced by monocrotaline and to explore its significance. Methods: Twenty-five male SD rats were randomly divided into control group ( n = 10) and monocretaline group ( n = 15). On the twenty-first day after the rats were intmperitoneally injected 60 mg/kg monoerotaline for monocrotaline group or equal volume vehicle for control group, the mean pulmonary artery pressure was measured by right heart catheterization. Histopathologieal study of lung tissue was done with hematoxylin-eosin (HE) and Masson' s trichrome staining. The eoneentmfion of apehn in the plasma was measured by radioimmunoassay. The expressions of apelin/APJ proteins and genes in lung tissue were measured respectively by Western blot and reverse transcription polymerase chain reaction (RT-PCR). Resalts: The mean pulmonary arterial pressure, right ventricular hypertrophy, pulmonary vascular remodeling index, content of apelin protein in lung tissue of monocrotaline group were higher than those in control group. APJ protein and gene expression in monocrotaline group were significantly lower than those in control group ( P 〈 0.01, P 〈 0.05), but apelin gene expression in the lung tissue between the two groups had no significant difference. Conclusion: Endogenous apelin/ APJ dysftmction may play an important role in the development of pulmonary hypertension induced by monocrotaline.
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