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. 2017 Dec 21;8:926. doi: 10.3389/fphar.2017.00926

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Copyright © 2017 Li, Zong, Zhang, Zhang, Xu, Liang, Yang, Yong and Qian.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Orientin ameliorates MI-induced oxidative stress. SOD (A) and NADPH oxidase (B) activity in the heart tissue of vehicle and orientin-treated mice (n = 6). (C) Immunohistochemistry staining of 4-hydroxynonenal (4-HNE) in the heart cross-sections of the vehicle and orientin-treated mice (n = 6). (D) The levels of lipid oxidation end products, malondialdehyde (MDA) in the indicated mice heart. (E–I) NRCMs were pretreated with orientin (1, 5, 15, 30 μM) for 12 h, then exposed to hypoxia for 24 h. The ROS was detected and quantified by DCFH-DA with light microscopy (E), ELISA reader (F). The levels of SOD (G), NADPH oxidase (H) activity, and malondialdehyde (I) in the indicated group (n = 6); ^∗p < 0.05 vs. vehicle-normoxia; ^#p < 0.05 vs. vehicle-hypoxia.