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. 2019 Aug 26;52(3):312–323. doi: 10.5115/acb.18.192

Fig. 2. Cyclosporin A (CsA) increases p53 activation and BH3 interacting-domain death agonist (BID) expression after H2O2 injury in human kidney proximal tubule epithelial cells. HK-2 cells were treated with either 10 nM CsA or vehicle for 60 minutes and then exposed to 1 mM H2O2 or control for 60 minutes (n=6 experiments per condition). (A) Phosphorylation level of p53 (p-p53, 53 kDa) and total expression level of p53 (t-p53, 53 kDa) were measured by western blot analysis. Antibody of β-actin (43 kDa) as a loading control was used for normalization. (B–D) Intensities of p-p53 and t-p53 protein bands were quantified using the AzureSpot software. (E) BID (22 kDa) expression was measured by western blot analysis. Antibody of β-actin (43 kDa) as a loading control was used for normalization. (F) Intensity of BID protein expression was quantified using the AzureSpot software. a)P<0.05 vs. control. b)P<0.05 vs. vehicle.

Fig. 2