目的:通过观察慢性低氧(O2)高二氧化碳(CO2)小鼠肺组织白细胞介素6(interleukin 6,IL-6)的表达水平变化,探讨其在慢性低O2高CO2肺动脉高压形成过程中的作用.方法:16只SPF级雄性C57BL/6小鼠按随机数字表法随机分为正常对照组和低氧高CO2组,每组8只.低氧高CO2组置于常压低O2高CO2舱内,O2浓度9%～10%,CO2浓度5%～6%,每天8 h,每周6 d,共4周.4周后,分离右心室和左心室加室间隔,计算右心肥大指数,肺组织行苏木精-伊红(HE)染色,光学显微镜观测肺血管结构变化,Image-Pro Plus 6.0图像分析系统测量管壁厚度占血管外径的百分比(WT%)和管壁面积占血管总面积的百分比(WA%).免疫组织化学方法观测肺动脉中IL-6蛋白的表达,ELISA测定肺组织匀浆中IL-6蛋白浓度;RT-PCR检测肺组织中IL-6 mRNA表达.结果:低氧高CO2组与对照组相比:(1)右心肥大指数、WT%和WA%显著提高(P<0.01);(2)肺组织中IL-6的蛋白表达水平显著提高(P<0.01);(3)肺组织中IL-6 mRNA表达水平明显提高(P<0.05).结论:在慢性低氧高二氧化碳环境中,小鼠的肺组织IL-6水平升高伴随肺血管壁肌层增厚和管腔狭窄,这可能与小鼠的肺动脉高压发生、发展有关.%AIM:To investigated the changes of interleukin - 6 ( IL - 6 ) in the pulmonary hypertension mice induced by chronic hypoxic hypercapnia. METHODS:Sixteen male C57BL/6 mice were randomly divided into 2 groups ( 8 mice in each group ); normal control group and chronic hypoxic hypercapnia group. The mice in chronic hypoxic hypercapnia group were placed in a sealed chamber where 02 concentration was kept at 9% -11%, and the CO2 concentration at 5% -6% , 8 h a day, 6 days a week for 4 weeks. The right ventricular ( RV ) weight, the weight of left ventricle plus ventricular septum ( LV + S ) were measured and right ventricular hypertrophy index [ RV/( LV + S ) ] was calculated. The structural changes of the pulmonary arteries were assessed by the method of histology with HE staining. The vessel wall diameter/total diameter ( WT% ) and the vessel wall area/total area ( WA% ) were analyzed by Image - Pro Plus 6. 0 software. The protein expression of IL-6 in the lungs of the mice was determined by I m muno hi sto chemistry and ELISA, and the mRNA expression of IL - 6 in the lungs was determined by RT - PCR. RESULTS: Compared with control group, RV/ ( LV + S), MT% , MA% and the expression of IL - 6 at mRNA and protein levels were significantly increased in chronic hypoxic hypercapnia group. CONCLUSION: In the environment of chronic hypoxia and hypercapnia, the expression of interleukin - 6 was elevated in mouse lungs, which may closely related to the development of pulmonary hypertension.
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