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. 2021 Mar 22;21:100. doi: 10.1186/s12906-021-03270-w

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — Tanshinone IIA (TIIA) + cyclosporine A (CsA) preserved myocardial mitochondrial function in renal ischemia-reperfusion (IR)-induced myocardial injury. The MMP (ratio of red/green), the opening of mPAP (%), the mitochondrial ROS, the mtDNA damage (ratio of long/short fragments), the mitochondrial RCR, mitochondrial oxygen consumption rate (a), the mitochondrial respiratory chain complex enzymes (I, II, III, IV, and V), and ATP (b) were recorded above. Rats were pre-treated with TIIA alone or in combination with CsA followed by removing the right kidney and clamping of the left renal artery for 30 min and reperfusion for 24 h. Sham rats were used as control. *p < 0.05 versus sham group, ^#p < 0.05 versus IR (obese) group, ^△p < 0.05 versus TIIA group, ^▲p < 0.05 versus CsA group