Gao Ziqing, Zhu Weiping, Zhang Hua, Li Zhonghe, Cui Tongxia
a Department of Ultrasound , the Fifth Affiliated Hospital of Sun Yat-Sen University , Zhuhai , China.
b Department of Nephrology , the Fifth Affiliated Hospital of Sun Yat-Sen University , Zhuhai , China.
Ren Fail. 2017 Nov;39(1):575-581. doi: 10.1080/0886022X.2017.1349677.
Renal fibrosis is a common pathway through which a variety of chronic kidney diseases progress to end-stage renal disease. Epithelial-mesenchymal transition (EMT) of renal proximal tubular cells is one of the most important factors in renal fibrosis. This study investigates if fasudil could influence EMT of renal proximal tubular cells.
HK-2 cells in passage 3-4 were used for all experiments. The cells were divided into five groups and treated with different concentrations of PTH and then observe cellular morphological changes at 0, 24 and 48 h using an inverted microscope and investigate the expression of the epithelial cell marker E-cadherin and the renal fibroblast marker α-smooth muscle actin (α-SMA).
PTH significantly induced EMT, fasudil-inhibited EMT induced by PTH to different degrees, and the inhibitory effect of fasudil was most pronounced at 20 μmol/L.
Monitoring PTH levels, early prevention and control of hyperparathyroidism and reducing the concentration of PTH are important means to improve prognosis and delay the progression of chronic kidney disease. Fasudil can restrain EMT induced by PTH; this conclusion provides experimental data for the application of fasudil in the clinical prevention and treatment of renal fibrosis.
肾纤维化是多种慢性肾脏病进展至终末期肾病的共同途径。肾近端小管上皮细胞的上皮-间质转化（EMT）是肾纤维化最重要的因素之一。本研究探讨法舒地尔是否能影响肾近端小管上皮细胞的EMT。
所有实验均采用第3-4代HK-2细胞。将细胞分为五组，用不同浓度的甲状旁腺激素（PTH）处理，然后在0、24和48小时使用倒置显微镜观察细胞形态变化，并研究上皮细胞标志物E-钙黏蛋白和肾成纤维细胞标志物α-平滑肌肌动蛋白（α-SMA）的表达。
PTH显著诱导EMT，法舒地尔不同程度抑制PTH诱导的EMT，法舒地尔在20μmol/L时抑制作用最明显。
监测PTH水平、早期防治甲状旁腺功能亢进及降低PTH浓度是改善慢性肾脏病预后、延缓其进展的重要手段。法舒地尔可抑制PTH诱导的EMT；这一结论为法舒地尔在肾纤维化临床防治中的应用提供了实验数据。
