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. 2016 Apr 5;13(5):4135–4142. doi: 10.3892/mmr.2016.5090

Figure 1.

Figure 1

VAS2870 inhibits radiation-induced fibroblastic changes in ECs. (A) HPAECs were irradiated with 5 Gy and incubated for 72 h. VAS2870 (1 µm) was added to cells 1 h prior to irradiation. To measure ROS, cells were incubated for 30 min with 1 µm 2′,7′-dichlorodihydrofluorescein diacetate and analyzed by flow cytometry (*P<0.05 vs. no VAS2870). (B) HPAECs were irradiated with 5 Gy and incubated for 72 h. VAS2870 (1 µm) was added to cells 1 h prior to irradiation and analysis by immunofluorescence with Alexa 488-conjugated anti-α-SMA and Alexa 594-conjugated anti-CD31 antibodies (green and red, respectively). Nuclei were counterstained with 4′,6-diamidino-2-phenylindole (blue) (scale bars, 20 µm). (C) Samples were subjected to western blot analysis of α-SMA, vimentin, CD31 and VE-cadherin. β-actin served as the loading control. Protein expression was quantified by densitometric analysis. Values are expressed as the mean ± standard deviation (n=3). *P<0.05 and **P<0.01 vs. VAS2870-untreated. HPAEC, human pulmonary artery endothelial cell; SMA, smooth-muscle actin; VAS, nicotinamide adenine dinucleotide phosphate oxidase inhibitor VAS2870; ROS, reactive oxygen species; VE, vascular endothelial.