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.%目的研究泛素羧基末端水解酶 L1（UCH-L1）在氟西汀抑制野百合碱诱导的大鼠肺动脉高压中的作用。方法用野百合碱（60 mg·kg －1）建立肺动脉高压大鼠模型，用低剂量（2 mg·kg －1·d －1）或高剂量（10 mg·kg －1·d －1）的氟西汀进行干预，观察各组大鼠血流动力学，肺组织与肺小动脉形态，以及 UCH-L1蛋白表达与核因子κB（NF-κB）核转位的变化。结果野百合碱诱导大鼠肺动脉压力升高、肺动脉重构、肺组织炎症反应、肺组织 UCH-L1表达减少以及 NF-κB 活性增加。氟西汀剂量依赖地抑制这些变化。但是各组之间大鼠肺动脉 UCH-L1蛋白表达差异无显著性。结论氟西汀抑制野百合碱诱导的大鼠肺组织炎症反应，与上调的UCH-L1蛋白抑制 NF-κB 活性有关。
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