Fig. 8: 11R-VIVIT attenuates TGFβ‑induced apoptosis in HK-2 cells.

a TGFβ treatment increased total NFAT2 expression in HK-2 cells. b TGFβ treatment decreased p-NFAT2 (Ser172) expression and 11R-VIVIT could increase the protein expression of p-NFAT2 (Ser172). c Quantification of NFAT2 expression normalized to GAPDH. d Quantification of p-NFAT2 (Ser172) expression normalized to GAPDH. e–f TGFβ treatment increased nuclear NFAT2 expression in HK-2 cells, and 11R-VIVIT inhibited the nuclear localization of NFAT2. g Quantification of NFAT2 expression in the cytoplasmic fraction HK-2 cells; The results were normalized to GAPDH. h Quantification of NFAT2 expression in the nuclear fraction of HK-2 cells; The results were normalized to Histone H3. i The protein expression of α-SMA and fibronectin in HK-2 cells. j–k The quantitative results of α-SMA and fibronectin were normalized to GAPDH. l Apoptosis was examined by flow cytometry. m Quantification of RTEC apoptosis by flow cytometry. n Western blot analysis of the expression of caspase-3 and C‑caspase-3 in HK-2 cells. o The quantitative results of caspase-3 and C‑caspase-3 were normalized to β-actin. p Western blot analysis of the expression of Bax in HK-2 cells. q The quantitative results of Bax were normalized to β-actin. r TUNEL staining of HK-2 cells in the CON, TGFβ and 11R-VIVIT + TGFβ group. s Quantification of TUNEL‑positive tubular epithelial cells. Scale bars = 20 μm. *P < 0.05 vs. TGFβ. TGFβ transforming growth factor beta, NFAT2 nuclear factor of activated T cells 2, p-NFAT2 phosphorylated nuclear factor of activated T cells 2, RTECs renal tubular epithelial cells, C‑caspase‑3 cleaved caspase‑3.