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. 2018 Nov 22;12:3985–3997. doi: 10.2147/DDDT.S184245

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© 2018 Han et al. This work is published and licensed by Dove Medical Press Limited

The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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SchB inhibited AngII-induced ROS generation and induced antioxidant responses in RAECs.

Notes: RAECs were pretreated with SchB (10 or 20 µM) for 1 hour and then incubated with AngII (1 µM) for the times indicated. After exposure to AngII for 12 hours, the effect of SchB on AngII-induced ROS generation in RAECs was determined by DCF (A) and DHE (C) staining, followed by semiquantitative analysis (B, D). DCF was rapidly deacetylated by cellular esterases and then oxidized in the presence of ROS into fluorescent DCF. DHE formed a red fluorescent product (ethidium) upon reaction with superoxide anions and intercalated with DNA. (E) Exposure to AngII for 8 hours. SchB induced an antioxidant response in RAECs, as evidenced by increased protein levels of Nrf2. GAPDH was used as loading control. (F–H) Exposure to AngII for 6 hours. mRNA expression of Nrf2 (F), Ho1 (G), and Nqo1 (H) was assessed in RAECs. mRNA levels were normalized to β-actin, and are shown relative to DMSO. ^*P<0.05, ^**P<0.01 compared to DMSO; ^#P<0.05, ^##P<0.01 compared to AngII. Magnification: 200× amplification (A and C).

Abbreviations: AngII, angiotensin II; DHE, dihydroethidium; DCF, 2’,7’ –dichlorofluorescin diacetate; DMSO, dimethyl sulfoxide; RAECs, rat aortic endothelial cells; SchB, schisandrin B.

SchB inhibited AngII-induced ROS generation and induced antioxidant responses in RAECs.

Notes: RAECs were pretreated with SchB (10 or 20 µM) for 1 hour and then incubated with AngII (1 µM) for the times indicated. After exposure to AngII for 12 hours, the effect of SchB on AngII-induced ROS generation in RAECs was determined by DCF (A) and DHE (C) staining, followed by semiquantitative analysis (B, D). DCF was rapidly deacetylated by cellular esterases and then oxidized in the presence of ROS into fluorescent DCF. DHE formed a red fluorescent product (ethidium) upon reaction with superoxide anions and intercalated with DNA. (E) Exposure to AngII for 8 hours. SchB induced an antioxidant response in RAECs, as evidenced by increased protein levels of Nrf2. GAPDH was used as loading control. (F–H) Exposure to AngII for 6 hours. mRNA expression of Nrf2 (F), Ho1 (G), and Nqo1 (H) was assessed in RAECs. mRNA levels were normalized to β-actin, and are shown relative to DMSO. ^*P<0.05, ^**P<0.01 compared to DMSO; ^#P<0.05, ^##P<0.01 compared to AngII. Magnification: 200× amplification (A and C).

Abbreviations: AngII, angiotensin II; DHE, dihydroethidium; DCF, 2’,7’ –dichlorofluorescin diacetate; DMSO, dimethyl sulfoxide; RAECs, rat aortic endothelial cells; SchB, schisandrin B.