FHL1和桩蛋白在低氧/炎症诱导形成肺动脉高压大鼠肺内的表达  

Expression of FHL1 and paxillin in lungs of rats with pulmonary hypertension induced by hypoxia/inflammation

作　　者：杨艳娟[1] 王海滨[2] 杨桂兰[2] 訾瑞[2] 王婷[2] 

机构地区：[1]宁夏医科大学总医院呼吸科,宁夏银川750004 [2]宁夏医科大学研究生院,宁夏银川750004

出　　处：《中国现代医学杂志》2015年第21期6-10,共5页China Journal of Modern Medicine

基　　金：宁夏自然科学基金(No:NZ1202)

摘　　要：目的了解FHL1和桩蛋白(Paxillin)在低氧/炎症条件下与肺血管重塑的关系。方法将40只Wistar雄性大鼠随机分为对照组、低氧组、百合碱组、低氧+百合碱组,每组10只,测大鼠平均肺动脉压力(m PAP)、右心室肥厚指数(RVHI)及肺小动脉相应管壁中膜厚度占其管径的百分比(WT%)。采用免疫组织化学染色法测定各组大鼠肺内FHL1、Paxillin的表达情况,并对肺组织切片进行图像分析。结果低氧组、百合碱组及低氧+百合碱组大鼠的m PAP与对照组相比均显著升高(均P<0.01),三组的RVHI与对照组相比均升高(均P<0.05),三组的WT%与对照组相比均显著升高(P<0.01)。低氧组、百合碱组及低氧+百合碱组三组大鼠的肺动脉FHL1免疫阳性染色分别为(0.16±0.03)、(0.15±0.03)、(0.21±0.03),与对照组(0.08±0.02)相比明显增强(均P<0.05);三组的Paxillin免疫阳性染色分别为(0.19±0.03)、(0.21±0.04)、(0.22±0.04),与对照组(0.11±0.03)相比明显增强(均P<0.05)。结论在缺氧/炎症诱导肺动脉高压形成的过程中FHL1、Paxillin均表达增加,可能在肺血管重塑和肺动脉高压的发病过程中起到一定的作用。【Objective】To investigate the role of four and a half LIM domain 1（FHL1） and paxillin in the occurrence of pulmonary vascular remodeling under the condition of low oxygen/inflammation. 【Methods】Forty male Wistar rats were randomly divided into four groups： control group, hypoxic model group, monocrotaline injection model group（MCT group） and monocrotaline injection with low oxygen treatment model group with 10 in each group.The mean pulmonary arterial pressure（m PAP）, the ratio of vascular wall area/total vascular area（WT%） and the index of right ventricular hypertrophy（RVHI） were measured. The expressions of FHL1 and paxillin in the lungs of rats were measured by immunohistochemical staining. 【Results】The m PAP of the hypoxic model group, the MCT group and the monocrotaline injection with low oxygen treatment model group was significantly increased compared with that of the control group（P 0.01）, the RVHI of the three groups was higher than that of the control group（P 0.05）. WT% of the three groups was significantly higher than that of the control group（P 0.01）. The positive staining of FHL1 of the three groups [（0.16 ± 0.03）,（0.15 ± 0.03）,（0.21 ± 0.03）, P 0.05] was significantly improved compared with that of the normal control group [（0.08 ± 0.02）], the positive staining of paxillin of the three groups[（0.19 ± 0.03）,（0.21 ± 0.04）,（0.22 ± 0.04）, P 0.05] was significantly higher than that of the control group [（0.11 ±0.03）].【Conclusions】FHL1 together with paxillin may play an important role in the pathogenesis of pulmonary vascular remodeling and pulmonary hypertension.

关 键 词：肺动脉高压 血管重塑 低氧 炎症 FHL1 桩蛋白 

分 类 号：R563[医药卫生—呼吸系统]