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. 2018 Mar 25;175(9):1548–1566. doi: 10.1111/bph.14164

Figure 4.

Figure 4

Aucubin inhibits oxidative stress and increases NO production in hypertrophic hearts and cardiomyocytes. (A–E) H9c2 cardiomyocytes were treated with aucubin (50 μM) and phenylephrine (PE; 50 μM) for 24 h. ROS were detected by DCFH‐DA with (A) light microscopy (n = 6 per experiment), (B) an elisa reader (n = 6 per experiment) and (C) flow cytometry (n = 6 per experiment) in the indicated groups. (D) Real‐time PCR analyses of oxidative markers (SOD, GPx and NADPH p67 phox, n = 6 per experiment). (E) NO production in the indicated groups (n = 6 per experiment). *P < 0.05 versus vehicle‐PBS group; #P < 0.05 versus vehicle‐phenylephrine group. All experiments were performed three independent times. (F) Immunohistochemical staining of 4‐hydroxynonenal in the indicated groups 4 weeks post‐AB surgery (n = 6 per experimental group). (G) RT‐PCR analyses of oxidative markers (SOD, GPx and NADPH p67 phox) in the indicated groups 4 weeks post‐AB surgery (n = 6 per experimental group). (H) NO production and SOD activation in the indicated groups 4 weeks post‐AB surgery (n = 6). *P < 0.05 versus vehicle‐sham; #P < 0.05 versus vehicle‐AB.