Fig. 9: Inhibition of SNO-USP16 at the C731 site improves cardiac dysfunction and GSH imbalance in CME rats.

A Cardiac function was evaluated using echocardiography. Detailed P values see (A). B Serum CK-MB level was measured using ELISA. Detailed P values see (B). C HBFP staining evaluated the microinfarct size in the heart tissues (scale bar = 100, 50 μm). The black arrow indicates a microsphere. Detailed P values see (C). D The pathological changes in the myocardial tissues were determined using HE staining (scale bar = 100, 50 μm). The black arrow indicates a microsphere, and the red arrow indicates inflammatory cell infiltration. Detailed P values see (D). E Apoptosis in the myocardial tissues was measured using TUNEL (scale bar = 100, 50 μm). Detailed P values see (E). F The expression of USP16, KDM1A, GCLM, and GLS in the myocardial tissues was analyzed using immunohistochemical staining (scale bar = 100, 50 μm). Detailed P values see (F). Data are presented as mean ± standard deviation (SD). n = 9 rats per group, indicating nine biological repetitions. In A, C–F, experiments were repeated independently at least 9 times with similar results. Representative images from one experiment are shown. One-way ANOVA followed by Tukey’s test for multiple group comparison was performed to analyze data. Source data are provided as a Source data file. SNO S-nitrosylation, USP16 ubiquitin-specific peptidase 16, GSH glutathione, CME coronary microembolization, CK-MB creatine kinase-MB, ELISA enzyme-linked immunosorbent assay, HE Hematoxylin-Eosin, TUNEL terminal deoxynucleotidyl transferase dUTP nick end labeling, KDM1A lysine-specific histone demethylase 1A, GCLM glutamate-cysteine ligase modifier subunit, GLS glutaminase, GSH glutathione.