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. 2021 Mar 3;21:121. doi: 10.1186/s12872-020-01742-4

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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. 5 — Overexpressed HMGB2 inverts the protective effects of miR-130a-5p on MIRI mice. a, b RT-qPCR and western blot analysis revealed that the mRNA expression and protein level of HMGB2 were evidently promoted when HMGB2 was up-regulated, n = 4. c, d EF, FS, LVSP and ± dp/dtmax were declined while LVEDP was enhanced when HMGB2 was up-regulated, n = 10. e CK and cTnT levels in serum were increased with up-regulated HMGB2 as detected using ELISA kits, n = 10. f myocardial injury was further deteriorated with up-regulated HMGB2 as detected by TUNEL assay, × 200, n = 6. g TUNEL assay suggested that the apoptosis rate of cardiomyocytes was enhanced with up-regulated HMGB2, × 400, n = 6. h Western blot analysis indicated that the Bax expression pattern was enhanced and the Bcl-2 expression pattern was reduced upon upregulated HMGB2, n = 4. The images of b, h shown are cropped. Two-way ANOVA was adopted to determine data in panels c, d, h, and one-way ANOVA was employed to determine data in panels a, b, d, e, g. Tukey’s multiple comparisons test was applied for post hoc test. **p < 0.01. HMGB high mobility group box, miR mircoRNA, MIRI myocardial ischemia reperfusion injury, RT-qPCR reverse transcription quantitative polymerase chain reaction, EF ejection fraction, FS fraction shortening, LVSP left ventricle systolic pressure, ± dp/dtmax maximal rate of rise and fall, LVEDP left ventricle end-diastolic pressure, CK creatine kinase, cTnT T Cardiac troponin T, TUNEL terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling, Bcl2 B-cell lymphoma-2, Bax Bcl2-Associated X, ANOVA analysis of variance