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中国应用生理学杂志 ›› 2016, Vol. 32 ›› Issue (5): 463-465.doi: 10.13459/j.cnki.cjap.2016.05.020

• 研究论文 • 上一篇    下一篇

低氧性肺动脉高压小鼠体内脂质水平的变化

范风云, 沈婉婷, 郑青青, 高媛, 胡凯媛, 范小芳, 毛孙忠, 龚永生   

  1. 温州医科大学低氧医学研究所, 浙江温州 325035
  • 收稿日期:2015-06-23 修回日期:2016-05-12 出版日期:2016-09-28 发布日期:2018-06-20
  • 通讯作者: 龚永生,Tel:0577-86699521;E-mail:fxbwzmc@126.com E-mail:fxbwzmc@126.com
  • 基金资助:
    浙江省自然基金(LY14H010005);浙江省大学生科技创新项目(2014R413029)

Changes of lipid levels in mice with hypoxic pulmonary arterial hypertension

FAN Feng-yun, SHEN Wan-ting, ZHENG Qing-qing, GAO Yuan, HU Kai-yuan, FAN Xiao-fang, MAO Sun-zhong, GONG Yong-sheng   

  1. Institute of Hypoxia Medicine, Wenzhou Medical University, Wenzhou 325035, China
  • Received:2015-06-23 Revised:2016-05-12 Online:2016-09-28 Published:2018-06-20
  • Supported by:
    浙江省自然基金(LY14H010005);浙江省大学生科技创新项目(2014R413029)

摘要: 目的:观察低氧性肺动脉高压小鼠体内脂质代谢的变化,探讨脂质代谢异常在低氧性肺动脉高压发生发展中的意义。方法:SPF级雄性C57BL/6小鼠20只,随机分为2组(n=10):常氧组和低氧组。常压连续低氧3周(9%~11% O2,23 h/d)复制慢性低氧性肺动脉高压模型,测定小鼠右心室压(RVSP)和右心室与左心室加室间隔重量比,Elisa法检测血浆中总胆固醇(TC)、低密度脂蛋白(LDL)、高密度脂蛋白(HDL)的含量;real-time PCR法检测肝组织中3-羟基-3-甲基戊二酸单酰辅酶A还原酶(HMGCR)、低密度脂蛋白受体(LDLR)、清道夫受体B1(SR-B1)、固醇调节元件结合因子2(SREBF2)等基因的表达。结果:低氧组小鼠RVSP、RV/(LV+S)显著高于常氧组(P<0.05),血浆中HDL含量及HDL/LDL比值较常氧组显著降低(P<0.05),肝组织中LDLR、SR-B1基因表达较常氧组显著下调(P<0.05);RVSP与HDL/LDL比值及LDLR、SR-B1基因表达呈显著负相关(P<0.05)。结论:脂质代谢异常参与小鼠低氧性肺动脉高压的形成。

关键词: 脂质代谢, 肺动脉高压, 低氧, 小鼠

Abstract: Objective: To observe the changes of lipid levels in mice with pulmonary hypertension induced by hypoxia. Methods: The animal model of hypoxic pulmonary hypertension was established by exposing the mice to isobaric hypoxic chamberfor 3 weeks (23 h/d, regular chow feed). Twenty male C57BL/6 mice were randomlydivided into normoxia group and hypoxia group (n=10). The concentrations of total cholesterol, low density lipoprotein (LDL) and high density lipoprotein (HDL) in plasma were detected by Elisa method.The mRNA levels of HMG-CoAreductase (HMGCR), low density lipoprotein receptor (LDLR), scavenger receptor class B1 (SR-B1), and sterol regulatory element-binding factor-2 (SREBF2) in liverwere measured by real-time PCR. Results: ① The right ventricular systolic pressure (RVSP) and the weight ratio of right ventricle (RV) to left ventricle plus septum (LV+S) of hypoxia group were significantly higher than those of normoxia group (P<0.05).② The concentrations of HDL and HDL/LDL in plasma were significantly higher in hypoxia group, compared with normoxia group (P<0.05).③The mRNA levels of LDLR and SR-B1in liver were significantly down-regulated in hypoxia group(P<0.05).④RVSP were significantly negative correlated with HDL/LDL, the gene expression of LDLR and SR-B1 (P<0.05). Conclusion: Abnormal lipid metabolism participates in the pathological proceeding of pulmonary hypertension induced by hypoxia.

Key words: lipid metabolism, pulmonary hypertension, hypoxia, mice

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