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. 2019 Jan 30;19(4):2581–2590. doi: 10.3892/mmr.2019.9908

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Copyright: © Qin et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 2. — RP decreases the oxidative stress and mPTP level of MI/R-induced cardiomyocytes. Cardiomyocytes were treated with MI/R, 20 µM RP+MI/R, 40 µM RP+MI/R and 80 µM RP+MI/R. (A) ROS levels were detected by flow cytometric analysis. (B) MDA content, (C) LDH activity, (D) SOD activity and (E) GPx activity in cardiomyocytes were measured using commercial kits. (F) Spectrophotometry was performed to detect the degree of mPTP openness in cardiomyocytes. ^#P<0.05 vs. Control; *P<0.05, **P<0.01 vs. MI/R. RP, rhynchophylline; mPTP, mitochondrial permeability transition pore; ROS, reactive oxygen species; MDA, malondialdehyde; LDH, lactate dehydrogenase; SOD, superoxide dismutase; GPx, glutathione peroxidase; MI/R, myocardial ischemia-reperfusion.