Artemisinin relieves myocardial ischemia-reperfusion injury via modulating miR-29b-3p and hemicentin 1

Figures

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  FIGURE 1. ARS suppresses H2O2-induced myocardial I/R injury. Proliferation, morphological changes, apoptosis, apoptosis-related protein, and oxidative stress biomarker in H9c2 cells via (A) CCK-8, (B) inverted phase contrast microscope (200 μm), (C) Flow cytometry, (D) Western blotting, (E) DCFH-DA (100 μm), (F) LDH Cytotoxicity Assay and (G) CK-MB isoenzyme assay, respectively. N = 3, *** p < 0.001 vs. Control; # p < 0.5, ### p < 0.001 vs. H2O2.

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  FIGURE 2. ARS systematically alters the gene expression profile of H9c2 cells. (A,B) The volcano plot of significant DEmiRNAs; (C,D) The miRNA-mRNA network.

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  FIGURE 3. MiR-29b-3p and HMCN1 are the target genes of ARS. (A) MiR-29b-3p and HMCN1 was determined; (B) Pearson’s correlation analysis was applied to analyze the relationship between miR-29b-3p and HMCN1. N = 3, *** p < 0.001 vs. Control; ### p < 0.001 vs. H2O2.

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  FIGURE 4. MiR-29b-3p and HMCN1 are the target genes of ARS on myocardial I/R injury. The expression of (A) miR-29b-3p and (B) HMCN1 in indicated groups tested using qRT-PCR; (C) Protein expression of HMCN1 evaluated via Western blotting. N = 3, ** p < 0.01, *** p < 0.001 vs. Control; ## p < 0.01, ### p < 0.001 vs. ARS or H2O2.

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  FIGURE 5. ARS suppresses myocardial I/R injury through regulating MiR-29b-3p/HMCN1. Proliferation, morphological changes, apoptosis, apoptosis-related protein and oxidative stress biomarker of H9c2 cells observed via (A) CCK-8, (B) inverted phase contrast microscope (200 μm), (C) Flow cytometry, (D) Western blotting, (E) DCFH-DA (100 μm), (F) LDH Cytotoxicity Assay and (G) CK-MB isoenzyme assay, respectively. N = 3, *** p < 0.001 vs. Control; ### p < 0.001 vs. H2O2; $$ p < 0.01, $$$ p < 0.001 vs. H2O2 + ARS; & p < 0.05, &&& p < 0.001 vs. H2O2 + ARS + miR-29b-3p inhibitor.

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  FIGURE 6. ARS suppresses myocardial I/R injury through regulating miR-29b-3p/HMCN1 in vivo.