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作 者:王佳兴[1] 唐发宽[1] 肖军[1] 华宁[1] 布伦[1] 王德水[1] 王洪叶[1]
出 处:《现代生物医学进展》2010年第13期2448-2450,共3页Progress in Modern Biomedicine
摘 要:目的:观察低氧性肺动脉高压大鼠肺内5-HT1B受体的分布和表达变化,探讨低氧性肺动脉高压的形成机制。方法:40只健康雄性SD大鼠随机分为正常组(control)、低氧3周组(2w)、低氧4周组(4w)和低氧5周组(5w)。除正常组外,其余3组大鼠分别在低氧环境中饲养3周、4周和5周。测定各组大鼠的平均肺动脉压力(mPAP)、右心室收缩压(RVSP)和右心室肥厚度[RV/(LV+S)%]。应用免疫组织化学法观察大鼠肺组织中5-HT1B受体的分布和表达,Westernblot法测定大鼠肺组织中5-HT1B受体的蛋白含量。结果:和正常组相比,低氧3周组大鼠的mPAP、RVSP和右心室肥厚度均显著升高(P均<0.05),并且随着低氧时间的延长而持续升高(P均<0.05)。免疫组织化学结果显示:5-HT1B受体主要分布在正常大鼠肺动脉的内膜层,而平滑肌层中仅有少量表达;和正常组相比,低氧3周组大鼠肺动脉平滑肌层中5-HT1B受体的表达显著增多;随着低氧时间的延长,大鼠肺动脉平滑肌层中5-HT1B受体表达持续增多。Westernblot结果表明,大鼠肺组织中5-HT1B受体的蛋白含量变化和免疫组织化学结果相一致。结论:低氧性肺动脉高压大鼠肺动脉中5-HT1B受体呈过度表达,这可能是低氧性肺动脉高压形成的分子机制之一。Objective:To investigate the changes of location and expression of 5-HT1B receptor in lung tissue of hypoxic pulmonary hypertension rats and to explore the mechanisms of hypoxic pulmonary hypertension(HPH).Methods:Forty male Sprague-Dawley rats were randomly divided into 4 groups:normoxia control(control),3w hypoxia(3w),4w hypoxia(4w) and 5w hypoxia(5w).The rats in normoxia control stayed in normal environment.The rats in 3w hypoxia,4w hypoxia and 5w hypoxia had been kept respectively in hypoxia chamber for 3 weeks,4 weeks and 5 weeks to establish the HPH animal model.After HPH rats were established,The mean pulmonary pressure(mPAP) and the right ventricular systolic pressure(RVSP) were recorded by a micro-catheter.RV/(LV + S) ratio was calculated to assess right vetricular hypertrophy.Location and expression of 5-HT1B receptor in lung tissues were measured by immunohistochemical and Western blot analyses.Results:Compared with normoxia control,mPAP,RVSP and RV/(LV + S)% of 3w hypoxia rats increased significantly(P〈0.05),which continued to increase following prolonged hypoxia.Immunohistochemistry shows that 5-HT1B receptor is localized mainly in the intima of the pulmonary arteries in normal rats.Exposed to hypoxia,immunoreactivity for 5-HT1B receptor increased in the media of 3w hypoxia rats' pulmonary arteries,particularly those bordering the adventitia.There were more changes in the expressions of 5-HT1B receptor following prolonged hypoxia.Western blot result showed the same changes of 5-HT1B receptor expressions in the lung tissues as that of 5-HT1B immunoreactivity in pulmonary arteries.Conclution:Hypoxia can induce the over-expression of 5-HT1B receptor in HPH rats' pulmonary arteries.It may be one of the underlying mechanisms of the development of HPH.
分 类 号:Q95-3[生物学—动物学] R541.4[医药卫生—心血管疾病]
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