脂肪因子CTRP9对大鼠高肺血流性肺动脉高压的影响  

Effects of adipokine CTRP9 on rats with pulmonary hypertension induced by high pulmonary blood flow

作　　者：张冠龙 马云飞 乔木 谢飞 王明杰 ZHANG Guanlong;MA Yunfei;QIAO Mu;XIE Fei;WANG Mingjie(Department of Internal Medicine-Cardiovascular,the 7th People's Hospital of ZhengZhou,Zhengzhou 450006,China)

机构地区：[1]郑州市第七人民医院心内科,450006

出　　处：《心肺血管病杂志》2020年第12期1506-1510,共5页Journal of Cardiovascular and Pulmonary Diseases

摘　　要：目的:探讨脂肪因子CTRP9对大鼠高肺血流性肺动脉高压的影响。方法:选取健康,3周龄,SD大鼠45只,采用随机分组法将大鼠分为:空白对照组、pAd空载组和pAd-CTRP9组,每组15只。空白对照组沿腹部正中切开后缝合;pAd空载组和pAd-CTRP9组经腹主动脉下腔静脉穿刺术建立高肺血流动物模型;pAd-CTRP9组完成造模后静脉注射pAd-CTRP9;采用ELISA测两组大鼠血清、肺组织中CTRP9水平;采用右心导管法测定肺动脉平均压;采用左颈总动脉插管测平均颈动脉压;检测大鼠肺动脉平滑肌中转化生长因子-β1(TGF-β1)和α平滑肌肌动蛋白(α-SMA)及PI3K/Akt信号通路蛋白表达水平;ELISA检测大鼠体内一氧化氮(NO)、内皮素(ET)和NO合的酶(eNOS)含量水平。结果:相比空白对照组,pAd空载组血清CTRP9、NO、ET和eNOS水平及肺组织中相关蛋白的相对表达水平,均差异无统计学意义(P>0.05)。相比pAd空载组,pAd-CTRP9组肺动脉平均压、TGF-β1和α-SMA水平均显著降低(P<0.05),血清CTRP9水平、肺组织中CTRP9水平、p-PI3K相对表达、p-Akt相对表达NO和eNOS水平均显著升高(P<0.05);ET水平、平均颈动脉压、PI3K相对表达、Akt相对表达,差异无统计学意义(P>0.05)。结论:CTRP9可以抑制平滑肌细胞增生、舒张血管、降低血压,缓解高肺血流性肺动脉高压大鼠模型高肺血流性和肺动脉高压。Objective:To explore the effects of adipokine CTRP9 on rats with pulmonary hypertension induced by high pulmonary blood flow.Methods:Forty-five healthy 3-week-old SD rats were enrolled and di-vided into blank control group,pAd no-load group and pAd-CTRP9 group by random grouping method,15 ca-ses in each group.In blank control group,rats were treated with incision and suture along the midline of the ab-domen.In pAd no-load group and pAd-CTRP9 group,animal models of high pulmonary blood flow were estab-lished through transabdominal aortic inferior vena cava(ⅣC)puncture.After modeling,pAd-CTRP9 group was injected intravenously with pAd-CTRP9.CTRP9 level in serum and pulmonary tissuess in both groups was measured by ELISA.The mean pulmonary arterial pressure(MPAP)was detected by right heart catheterization method.The mean carotid arterial pressure(MCAP)was detected by left common carotid artery intubation.The expression levels of transforming growth factor-β1(TGF-β1),αsmooth muscle actin(α-SMA)and PI3K/Akt signaling pathway proteins in pulmonary artery smooth muscle were detected.The contents of nitric oxide(NO),endothelin(ET)and endothelial NO synthase(eNOS)were detected by ELISA.Results:Com-pared with blank control group,the differences in levels of serum CTRP9,NO,ET and eNOS,and relative ex-pression levels of related proteins in pulmonary tissues in pAd no-load group were not statistically significant(P>0.05).Compared with pAd no-load group,MPAP,levels of TGF-β1 andα-SMA were significantly decreased in pAd-CTRP9 group(P<0.05),while level of CTRP9 in serum and pulmonary tissues,relative expression of p-PI3K and p-Akt,levels of NO and eNOS were significantly increased(P<0.05).And there were no signifi-cant differences in ET level,MCAP,relative expression of PI3K and Akt between the two groups(P>0.05).Conclusions:CTRP9 can inhibit proliferation of smooth muscle cells,relax vessels,lower blood pressure,al-leviate high pulmonary blood flow and pulmonary hypertension in the rat models with pulmonary hypertension

关 键 词：肺动脉高压 CTRP9 肺动脉 高肺血流动物模型 

分 类 号：R54[医药卫生—心血管疾病]