天津医药

天津医药 ›› 2020, Vol. 48 ›› Issue (7): 621-624.doi: 10.11958/20193959

• 实验研究 • 上一篇    下一篇

miR-322对大鼠高原性肺动脉高压的作用及机制研究

张凤涛1 ，李晓红2 ，王景景2 ，孙洪涛2 ，陈翀2 ，陈锋3△   

  1. 1 天津理工大学化学化工学院（邮编 300384）；2 武警特色医学中心神经创伤及修复研究所；3 天津医科大学博士后工作站
  • 收稿日期:2019-12-30 修回日期:2020-03-25 出版日期:2020-07-15 发布日期:2020-07-16
  • 作者简介:张凤涛（1990），男，硕士在读，主要从事高原肺水肿发病机制研究

The effect and mechanism of miR-322 on high altitude pulmonary hypertension in rats

ZHANG Feng-tao1 , LI Xiao-hong2 , WANG Jing-jing2 , SUN Hong-tao2 , CHEN Chong2 , CHEN Feng3△   

  1. 1 School of Chemistry and Chemical Engineering, Tianjin University of Technology, Tianjin 300384, China; 2 Institute of Neurotrauma Repair of Characteristic Medical Center of PAP; 3 Postdoctoral Workstation of Tianjin Medical University
  • Received:2019-12-30 Revised:2020-03-25 Published:2020-07-15 Online:2020-07-16

PDF (PC)

4330

摘要： 目的 探讨miR-322对高原肺动脉高压发生发展的影响及作用机制。方法 SPF级雄性SD大鼠40只，随 机数字表法分为4组（n=10），即常氧组、低氧组、空白病毒+低氧组（空载体组），miR-322抑制+低氧组（miR-322沉默 组），剔除实验过程中死亡大鼠后常氧组 10 只，低氧组、空载体组、miR-322 沉默组各 9 只。测定肺动脉氧分压 ［p（O2 ）］和平均肺动脉压（mPAP）；HE染色观察肺组织变化；免疫荧光观察组织α-平滑肌肌动蛋白（α-SMA）表达变 化；实时荧光定量PCR检测大鼠肺组织中miR-322和apelin mRNA基因表达；Western blot法检测大鼠肺组织中apelin 蛋白的表达。结果 低氧组和空载体组肺动脉p（O2 ）、mPAP和肺组织各项指标差异均无统计学意义。与常氧组比 较，低氧组mPAP、α-SMA、apelin mRNA和蛋白以及miR-322 mRNA相对表达量均升高，p（O2 ）下降（P＜0.05）；肺组织 破坏严重，大量炎症细胞浸润。与低氧组比较，miR-322 沉默组 mPAP 和 miR-322 mRNA 相对表达量均下降，α- SMA、p（O2 ）以及apelin mRNA和蛋白相对表达量上升（P＜0.05）；肺组织损伤程度降低。结论 抑制miR-322表达可 促进高原肺动脉高压模型大鼠apelin的表达，进而降低高原肺动脉高压的上升程度。

关键词: 高血压, 肺性；高原病；疾病模型, 动物；miR-322；apelin

Abstract: Objective To explore the effect and mechanism of miR-322 on the occurrence and development of pulmonary hypertension at high altitude. Methods Forty SPF male rats were randomly divided into 4 groups (n=10): normoxic group (Normoxia), hypoxia group (Hypoxia), blank virus + hypoxia group (no load group) and miR-322 inhibition + hypoxia group (miR-322 group). The dead rats during the experiment were excluded, and eventually there were 10 rats in normoxic group, 9 rats in hypoxia group, empty load group and miR-322 group respectively. The pulmonary arterial oxygen partial pressure [p (O2)] and mean pulmonary artery pressure (mPAP) were measured. HE staining was used to observe the changes of lung tissue. The expression of α-SMA was observed by immunofluorescence. miR-322 and apelin mRNA gene expressions in rat lung tissues were detected by real-time PCR. The expression of apelin protein in rat lung tissue was detected by Western blot assay. Results There were no significant differences in p (O2), mPAP and indicators of lung tissues between hypoxia group and no-load group. Compared with the normoxic group, the relative expressions of mPAP, α- SMA, apelin protein and miR-322 were increased, and p (O2) was decreased in the hypoxia group (P＜0.05). The lung tissues were severely damaged and a large number of inflammatory cells infiltrated. Compared with hypoxia group, the relative expressions of mPAP and miR-322 were decreased in miR-322 group, the p (O2) in pulmonary artery and the relative expression of apelin protein increased, α-SMA and lung tissue damage decreased (P＜0.05). Conclusion The inhibition of miR-322 expression promotes the expression of apelin in rats with high altitude pulmonary hypertension and reduces the rise of high altitude pulmonary hypertension.

Key words: hypertension, pulmonary, altitude sickness, disease models, animal, miR-322, apelin