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| The effect and mechanism of icariin on the epithelial-mesenchymal transdifferentiation of renal tubular epithelial cells induced by TGF-β1 |
| Hits 572 Download times 276 Received:February 26, 2022 |
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| DOI
10.11656/j.issn.1673-9043.2022.04.15 |
| Key Words
transforming growth factor-β1;renal tubular epithelial cell;icariin;epithelial-mesenchymal transition;Smad signaling pathway |
| Author Name | Affiliation | | WANG Shenwei | Department of Nephrology, Xuchang Central Hospital Affiliated to Henan University of Science and Technology, Xuchang 461000, China | | WANG Qiong | Department of Nephrology, Xuchang Central Hospital Affiliated to Henan University of Science and Technology, Xuchang 461000, China | | CHEN Juntong | Department of Nephrology, Xuchang Central Hospital Affiliated to Henan University of Science and Technology, Xuchang 461000, China | | ZHAO Yanyan | Department of Endocrinology, the First Affiliated Hospital of Zhengzhou University,Zhengzhou 450000, China |
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| Abstract
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| [Objective] To observe the effect of icariin on the renal tubular epithelial-mesenchymal transition induced by TGF-β1 and its influence on the Smad signaling pathway.[Methods] Renal tubular epithelial cells(HK-2) were divided into blank control group, TGF-β1 group, and TGF-β1+icariin(10, 20, 40 μmol/L) group. We used CCK-8 method to detect the effect of 10, 20, 40 μmol/L icariin on the proliferation of renal tubular epithelial cells induced by 10 μg/L TGF-β1;RT-qPCR method to detect epithelial-mesenchymal transition in charge of the key factors α-smooth muscle actin(α-SMA), E-cadherin, vimentin mRNA expression; Western blot to detect α-SMA, E-cadherin, Smad2/3 and p-Smad2/3 protein expression; and scratch test and invasion and migration chamber method(Transwell chamber) to detect the migration and invasion ability of HK-2 cells.[Results] Compared with the blank control group, the HK-2 cell proliferation, migration and invasion ability of the TGF-β1 group were significantly increased(P<0.05), and the expression of α-SMA, vimentin protein and mRNA, and p-Smad2/3 protein were significantly increased(P<0.05), while the expression of E-cadherin, Smad2/3 protein and mRNA were significantly reduced(P<0.05). Compared with the TGF-β1 group, the HK-2 cell proliferation, migration and invasion ability of the TGF-β1+ icariin(10, 20, 40 μmol/L) group were significantly reduced(P<0.05), α-SMA, vimentin protein, mRNA and p-Smad2/3 protein expression were decreased significantly(P<0.05), while E-cadherin, Smad2/3 protein and mRNA expression were increased significantly(P<0.05). Icariin had not a dose-dependent effect on the ability of TGF-β1 to induce HK-2 cells to inhibit proliferation, migration and invasion, and epithelial-mesenchymal transition.[Conclusion] Icariin could inhibit TGF-β1 induced differentiation of epithelial-mesenchymal transition of HK-2 cells, which may be related to the inhibition of Smad signaling pathway. |
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