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作 者:舒鹰[1] 李秋[1] 李云雷[1] 张丽萍[1] 陈成水[1]
机构地区:[1]温州医学院附属第一医院呼吸内科,浙江温州325000
出 处:《中国应用生理学杂志》2011年第3期311-314,共4页Chinese Journal of Applied Physiology
基 金:浙江省自然科学基金资助项目(Z2080988)
摘 要:目的:研究线粒体ATP敏感钾通道(mitoKATP)抑制剂5-羟基癸酸盐(5-HD)对慢性低氧肺动脉高压大鼠的影响及其潜在机制。方法:雄性SD大鼠48只,随机分成4组(n=12):①正常对照组;②慢性低氧组;③慢性低氧+5-HD组;④慢性低氧+Diazoxide(mitoKATP开放剂)组;除正常对照组外,其余3组置于氧舱内(氧浓度10%±0.3%),每天低氧8 h,并接受不同的干预,共4周。干预结束后右心导管法测各大鼠肺动脉压,RT-PCR和Westernblot检测各组大鼠肺动脉PKC-ɑ蛋白和mRNA的表达。结果:①慢性低氧组肺动脉压显著高于正常组(P<0.01),同时慢性低氧+Diazoxide组与慢性低氧+5-HD组肺动脉压较慢性低氧组显著减低(P<0.01)。②慢性低氧组PKC-ɑ蛋白及mRNA的相对表达显著高于正常组(P<0.05)。结论:5-HD对慢性低氧肺动脉高压起保护作用,其机制可能是抑制线粒体ATP敏感钾通道。Objective: To investigate the effect of mito chondrial KATP channels (mitoKATP) inhibitor 5-hydroxydecanoate(5-HD) on chronic hypoxic pulmonary artery hypertension (CI-IPAH) rats and its underlying mechanisms. Methods: Forty-eight male SD rats were equally divided into 4 groups randomly( n = 12) : normal group, hypoxia group, hypoxia + 5-HD group, hypoxia + Diazoxide group. Except the first group, the other three groups were put into hypoxic [ O2(10.0% ±0.3% ] and normobaric chamber for four weeks to establish chronic hypoxic model and received different interference. When the interference completed, right heart catheter was used to detect the mean ptdmonary arterial pressure(mPAP) of each rat and PKC-αmRNA expression in pulmonary arteries was detected by reverse transcription -polymerase chain reaction (RT- PCR) and protein expression by Western blot. Results: (1)mPAP was much higher in hypoxia group than that in normal group( P 〈 0. 01) while in hypoxia + 5-HD group and hypoxia + diazoxide were decreased significantly compared to hypoxia group( P 〈 0.01). (2) The protein and mRNA levels of PKC-n in the hypoxic group were higher than those in normal group( P 〈 0.05). Conclusion: 5-HD plays a protective role on CHPAH. The mechanism of its effect may be attributed to inhibiting MitoKATP.
关 键 词:慢性低氧肺动脉高压 PKC-Α 线粒体ATP敏感钾通道 5-HD
分 类 号:R331[医药卫生—人体生理学]
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