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. 2022 Aug 17;13:964370. doi: 10.3389/fphar.2022.964370

FIGURE 4.

FIGURE 4

SKI improved morphological changes and injury in AngII-induced HK-2 cells. (A) Cell viability analysis after HK-2, NRK-52E and NRK-49F cells were treated with increasing concentrations of SKI (0–16 mg/ml). (B) Morphological observation in AngII-induced HK-2 cells treated with different concentrations of SKI (0–6.0 mg/ml) and losartan (1.0 mM) at 48 h. (C) Protein expression of α-SMA and fibronectin in AngII-induced HK-2 cells treated with different concentrations of SKI (0.25, 0.5, 1.0, 2.0 mg/ml). (D) Quantitative analysis of the protein expression of α-SMA and fibronectin in AngII-induced HK-2 cells treated with different concentrations of SKI (0.25, 0.5, 1.0, 2.0 mg/ml) for 48 h. (E) Protein expression of collagen I and E-cadherin in AngII-induced HK-2 cells treated with SKI. (F) Quantitative analysis of the protein expression of collagen I and E-cadherin in AngII-induced HK-2 cells treated with SKI. (G) Representative immunofluorescent analysis of fibronectin in AngII-induced HK-2 cells treated with SKI. (H) Protein expression of collagen I, α-SMA, E-cadherin and fibronectin in AngII-induced NRK-49F cells treated with SKI. (I) Quantitative analysis of the protein expression of collagen I, α-SMA, E-cadherin and fibronectin in AngII-induced NRK-49F cells treated with SKI. *p < 0.05, **p < 0.01 compared with the control group; # p < 0.05, ## p < 0.01 compared with the AngII-induced group.