CAJ | 학술논문

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。
목적연구범소최기말단수해매 L1（UCH-L1）재불서정억제야백합감유도적대서폐동맥고압중적작용。방법용야백합감（60 mg·kg －1）건립폐동맥고압대서모형，용저제량（2 mg·kg －1·d －1）혹고제량（10 mg·kg －1·d －1）적불서정진행간예，관찰각조대서혈류동역학，폐조직여폐소동맥형태，이급 UCH-L1단백표체여핵인자κB（NF-κB）핵전위적변화。결과야백합감유도대서폐동맥압력승고、폐동맥중구、폐조직염증반응、폐조직 UCH-L1표체감소이급 NF-κB 활성증가。불서정제량의뢰지억제저사변화。단시각조지간대서폐동맥 UCH-L1단백표체차이무현저성。결론불서정억제야백합감유도적대서폐조직염증반응，여상조적UCH-L1단백억제 NF-κB 활성유관。
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.