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