肺动脉高压大鼠模型肺血管维甲酸受体的变化

摘要

Objective To interpret the relationship of retinoic acid receptor (RAR) and pathogenesis of pulmonary hypertension (PH), and evaluate the reverse effect of all-trans retinoic acid (atRA) on pulmonary vessel of PH. Methods Seventy-two SD rats of 3 week old were selected and divided into three groups randomly. The group 1 was SD rat with PH induced by monocrotaline, group 2 was SD rat induced by monocrotaline and was administered orally by gavage with atRA 10 mg/(kji;-d) , and control group with saline. The mean pulmonary artery pressure was measured in 6 cases in each group on day 7, 14, 21, 28, and number of RAR and mRNA level of the pulmonary artery and lung were detected by real-lime quantitative polymerase chain reaction. Results The RAR (α β and γ) transcription in pulmonary vascular decreased when the rat was with PH and decreased more apparently as PH became serious. Conclusions RAR may participate in the pathogenesis of PH.%目的 闸明维甲酸受体(retinoicacid receptor,RAR)变化与肺动脉高压发病机制的关系,并评价全反式维甲酸(all-trans retinoic acid,atRA)对肺高压肺血管重建过程的逆转作用.方法 选择3周龄SD大鼠72只,将其平均分为3组,试验组1为野百合碱( Monocrotaline,MCT)诱导建立SD大鼠肺动脉高压模型；试验组2为MCT诱导建立SD大鼠,同时给予atRA 10 mg/(kg·d)灌胃；对照组为生理盐水组.分别于实验第7、14、21、28天每组取6只大鼠,测肺动脉压力后处死；实时定量RT-PCR检测主动脉、肺动脉及肺组织中RAR受体数量与mRNA水平.结果 肺动脉高压时,肺血管中RAR各亚型(α、β、γ)转录水平均有下降,且随肺动脉高压加重下降更为明显.结论 RAR可能参与了肺动脉高压的发病机制.