Fig. 8
C3G regulated NDRG2 expression, EMT and extracellular matrix deposition through the PI3K/AKT pathway in HK-2 cells. (A-B) The expression of PI3K, p-PI3K, AKT, p-AKT and the quantification were shown after C3G treatment in TGF-β1 induced HK-2 cells. (C) Western blot and quantification of the effect of the combination of C3G and SC79 (PI3K activator, 20 µM) on PI3K/AKT expression. (D) The combination of C3G and SC79 (PI3K activator, 20 µM) could reverse the increased NDRG2 expression induced by C3G on TGF-β1 treated HK-2 cells. (E) The combination of C3G and SC79 (PI3K activator, 20 µM) could reverse the increased EMT induced by C3G on TGF-β1 treated HK-2 cells. (F) The combination of C3G and SC79 (PI3K activator, 20 µM) could reverse the increased extracellular matrix deposition induced by C3G on TGF-β1 treated HK-2 cells. Values were expressed as the mean ± SEM. *P < 0.05, relative to the control group. #P < 0.05, relative to the TGF-β1 + C3G group.
