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泛素羧基末端水解酶 L1在氟西汀抑制大鼠肺动脉高压中的作用

王寒明 王怀良 艾秀丽 白洋 王韵

中国药理学通报Issue(9):1244-1248,5.
中国药理学通报Issue(9):1244-1248,5.DOI:10.3969/j.issn.1001-1978.2015.09.013

泛素羧基末端水解酶 L1在氟西汀抑制大鼠肺动脉高压中的作用

Role of UCH-L1 in protection of fluoxetine against pulmonary arterial hypertension in rats

王寒明 1王怀良 2艾秀丽 3白洋 4王韵5

作者信息

  • 1. 辽宁医学院药理学教研室,辽宁 锦州 121001
  • 2. 中国医科大学药学院临床药理教研室
  • 3. 中国医科大学药学院临床药理教研室
  • 4. 中国医科大学呼吸疾病研究所
  • 5. 中国医科大学心血管疾病研究所,辽宁 沈阳 110001
  • 折叠

摘要

Abstract

Aim To study the role of ubiquitin carboxyl terminal hydrolase L1 (UCH-L1)involved in the pro-tective effect of fluoxetine against monocrotaline-in-duced pulmonary arterial hypertension in rats.Meth-ods Monocrotaline (60 mg·kg -1 )was used to es-tablish pulmonary arterial hypertension in rats and low-dose (2 mg·kg -1 ·d -1 )or high-dose (10 mg·kg -1 ·d -1 )fluoxetine was applied to inhibit pulmonary ar-terial hypertension.The hemodynamics,morphology of pulmonary arterioles and lungs,UCH-L1 protein ex-pression and nuclear factor-κB (NF-κB)nuclear trans-location were observed.Results Monocrotaline not only increased pulmonary arterial pressure and promo-ted pulmonary arterial remodelling and lung inflamma-tion,but also down-regulated UCH-L1 protein expres-sion and increased NF-κB activity in lungs.Fluoxetine inhibited these changes in a dose-dependent manner. However,UCH-L1 protein expression of pulmonary ar-teries did not significantly change among different groups.Conclusion Fluoxetine inhibits monocrotal-ine-induced lung inflammation in rats,involved in NF-κB activity inhibited by up-regulated UCH-L1 protein expression.

关键词

泛素羧基末端水解酶 L1/肺动脉高压/氟西汀/核因子 κB/炎症/野百合碱

Key words

ubiquitin carboxyl terminal hydrolase L1/pulmonary arterial hypertension/fluoxetine/nuclear factor-κB/inflammation/monocrotaline

分类

医药卫生

引用本文复制引用

王寒明,王怀良,艾秀丽,白洋,王韵..泛素羧基末端水解酶 L1在氟西汀抑制大鼠肺动脉高压中的作用[J].中国药理学通报,2015,(9):1244-1248,5.

基金项目

国家自然科学基金资助项目(No 81273511);辽宁省科技厅博士启动基金项目(No 20131066);辽宁医学院奥鸿博泽基金项目 ()

中国药理学通报

OA北大核心CSCDCSTPCD

1001-1978

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