CAJ | 학술논문

目的：探讨miRNA-29b（简称miR-29b）在特发性肺间质纤维化（IPF）上皮间充质转分化（EMT）过程中的抗纤维化作用。方法：将体外培养的IMR-90细胞随机分为空白对照组、TGF-β1诱导组（诱导48 h）、miR-29b转染组（TGF-β1＋miR-29b）和miR-29b阴性对照组（TGF-β1＋无意义序列）；应用倒置相差显微镜观察细胞形态改变；运用实时荧光定量PCR技术和Western bolt技术分别检测TGF-β／Smad信号通路Smad3和p-Smad3、上皮标志物E-钙黏蛋白（E-cad）、间质标志物平滑肌肌动蛋白（α-SMA）和下游靶基因Ⅰ型胶原蛋白（COL1A1）的表达。结果：与空白对照组比较，TGF-β1诱导组IMR-90细胞中E-cad表达显著下降，p-Smad3、α-SMA和COL1A1的表达显著升高（P均＜0．05）；与TGF-β1诱导组比较，miR-29b转染组E-cad表达升高，p-Smad3、α-SMA和COL1A1的表达降低（P均＜0．01）。结论：上调miR-29b表达可抑制TGF-β／Smad信号通路介导的肺泡上皮细胞EMT。
목적：탐토miRNA-29b（간칭miR-29b）재특발성폐간질섬유화（IPF）상피간충질전분화（EMT）과정중적항섬유화작용。방법：장체외배양적IMR-90세포수궤분위공백대조조、TGF-β1유도조（유도48 h）、miR-29b전염조（TGF-β1＋miR-29b）화miR-29b음성대조조（TGF-β1＋무의의서렬）；응용도치상차현미경관찰세포형태개변；운용실시형광정량PCR기술화Western bolt기술분별검측TGF-β／Smad신호통로Smad3화p-Smad3、상피표지물E-개점단백（E-cad）、간질표지물평활기기동단백（α-SMA）화하유파기인Ⅰ형효원단백（COL1A1）적표체。결과：여공백대조조비교，TGF-β1유도조IMR-90세포중E-cad표체현저하강，p-Smad3、α-SMA화COL1A1적표체현저승고（P균＜0．05）；여TGF-β1유도조비교，miR-29b전염조E-cad표체승고，p-Smad3、α-SMA화COL1A1적표체강저（P균＜0．01）。결론：상조miR-29b표체가억제TGF-β／Smad신호통로개도적폐포상피세포EMT。
Aim: To explore the antifibrotic effect of miR-29b in the process of epithelial-mesenchymal transition (EMT) in idiopathic pulmonary fibrosis (IPF).Methods: IMR-90 cells cultured in vitro were randomly allocated into blank control group, TGF-β1-induced group, miR-29b transfection group(TGF-β1+miR-29b) and negative control group ( TGF-β1+NC) .The expressions of markers of epithelial cell and mesenchymal cell were detected by real -time PCR and Western blot , and the cellular morphological changes of IMR-90 cells before and after the transfection were observed by in-verted phase contrast microscope .Results: E-cad expression significantly decreased and α-SMA, p-Smad3 and COL1A1 expression significantly increased in TGF-β1-induced group compared with blank control group (P<0.05).E-cad expres-sion was increased and α-SMA, p-Smad3 and COL1A1 expression were decreased in miR-29b transfection group compared with TGF-β1-induced group(P<0.01).Conclusion: Upregulation of miR-29b may inhibit the TGF-β/Smad signaling pathway mediated EMT , and delay the progression of IPF .