Fig.4

SIK1 was down-regulated in AA-treated HK2 cells and overexpression of SIK1 improved AA-induced HK2 cells injury. a ELISA detection of IL-1β and TNF-α levels in the supernatant of HK2 cells treated with 10 μmol/L AA for 0 h, 24 h, 48 h and 72 h. b Western blot analysis of Caspase 1/p20/p10, E-cadherin, ZO-1, Vimentin, and α-SMA protein levels in HK2 cells treated with 10 μmol/L AA for 0 h, 24 h, 48 h and 72 h, with the greatest effect after 72 h of treatment. β-actin was used as a control. c real-time PCR analysis of early fibrosis indicators (COLI, PAI-1, and MMP9) mRNA levels in HK2 cells treated with 10 μmol/L AA for 72 h. d Western blot analysis of p-SIK1(Thr182) and SIK1 levels in HK2 cells treated with 10 μmol/L AA for 0 h, 24 h, 48 h and 72 h. e Western blot analysis of Caspase1/p20/p10, E-cadherin, Vimentin, Fsp1, and COL1 in HK2 cells that are treated with SIK1 vector (SIK1 lentiviral overexpression vector) in the presence of 10 µmol/L AA or treated with 10 µmol/L AA alone for 72 h. f Representative immunofluorescence images of E-cadherin and Vimentin in HK2 cells. Scale bar = 50 μm. g Representative migration results of HK2 cells. Scale bar = 50 μm. Data are shown as mean ± s.d. *P < 0.05 vs Control, ^#P < 0.05 vs AA. All experiments were performed in triplicate