山东医药2017，Vol.57Issue(13)：20-23,4.DOI:10.3969/j.issn.1002-266X.2017.13.006
rBMSCs/ F92A-Cav1对PAH大鼠的治疗作用及其机制
Therapeutic effect and mechanism of rBMSCs/F92A-Cav1 on PAH rats
摘要
Abstract
To investigate the therapeutic effect and mechanism of Caveolin-1 (Cav1) mutant to F92A-Cav1 modified rat bone marrow mesenchymal stem cells (rBMSCs/F92A-Cav1) on rats with pulmonary hypertension (PAH).Methods PAH was induced by intraperitoneal injection of 1% monocrotaline (MCT, 60 mg/kg) in adult male Wistar rats.The PAH rats were randomly divided into four groups (10 rats/group) after 2 weeks of MCT injection: PAH group (only MCT), Cav1 group (transduced with LV-Cav1 modified rBMSCs), F92A-Cav1 group (transduced with LV-F92A-Cav1modified rBMSCs), and the control group.Gene modified rBMSCs (1×106/ml) were transplanted into PAH rats in each group by tail vein injection.After 3 weeks of transplantation, the percentage of media wall thickness (MT%) and right ventricular hypertrophy index (RVHI) were evaluated by Image-Pro Plus 6 software, serum NO concentration was checked by Griess method, and the expression of phosphoinositide 3-kinase(PI3K) and protein kinase B (AKT) was detected by Western blotting.Results MT%, RVHI, PI3K and AKT was all increased but NO was decreased in the PAH group as compared with that of the control group(P<0.05 or P<0.01).Compared with the PAH group, MT%, RVHI, PI3K and AKT was decreased but NO was increased in the Cav1 and F92A-Cav1 groups, especially in the F92A-Cav1 group (P<0.01).Conclusion F92A-Cav1 can abrogate the inhibitory effect of wild-type Cav1 on eNOS and promote the release of NO, then inhibit the activation of PI3K/Akt signaling pathway and thus exert its therapeutic effect on PAH rats.关键词
肺动脉高压/窖蛋白-1/骨髓间充质干细胞/大鼠Key words
pulmonary arterial hypertension/Caveolin-1/mesenchymal stem cells/rats分类
医药卫生引用本文复制引用
徐聪,陈海英,夏鹏,杨红莉,唐文强,潘丽,王兰花,陈双峰,张颖新,王乐信..rBMSCs/ F92A-Cav1对PAH大鼠的治疗作用及其机制[J].山东医药,2017,57(13):20-23,4.基金项目
国家自然科学基金资助项目(81270104) （81270104）
山东省自然科学基金资助项目(ZR2016HP33). （ZR2016HP33）
