Background Patients of coronary artery disease (CAD) with type 2 diabetes mellitus (DM2) show increased mortality risk than CAD patients without DM2, while few biomarkers can be used to discriminate them. Methods Fifty‐nine patients of CAD with DM2 (DM2‐CAD group), 79 patients of CAD without DM2 (CAD group), and 63 healthy control subjects were recruited. Circulating miR‐130 (miR‐130a and miR‐130b) and PPAR‐γ (peroxisome proliferator‐activated receptor gamma) were measured and their Pearson correlation was analyzed. 3′ UTR binding prediction and luciferase assay were used to determine the target relationship between miR‐130 and PPAR‐γ. Receiver operating characteristics (ROC) analysis was performed to test the discrimination ability of miR‐130 between DM2‐CAD and CAD groups. Results miR‐130a and miR‐130b showed decreased expression in DM2‐CAD group when compared with the CAD group and health control. Both bioinformatics and luciferase assays showed that miR‐130 could bind the 3′ UTR of PPAR‐γ. Furthermore, miR‐130 negatively correlated with PPAR‐γ in both CAD and DM2‐CAD group in Pearson's coefficient analysis. Both miR‐130a and miR‐130b were able to discriminate DM2‐CAD group from CAD group and control subjects. Conclusion Circulating miR‐130 may regulate the expression of PPAR‐γ and can be used as a biomarker to discriminate DM2‐CAD from CAD.

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Coronary microembolization (CME)‐induced inflammation and cardiomyocyte apoptosis are two key factors contributing to CME‐induced myocardial dysfunction. High‐mobility group box‐1 (HMGB1) plays essential role in progression of CME‐induced injury and inhibition of HMGB1 has been shown to be protective. In present study, the potential effects of glycyrrhizin, a HMGB1 inhibitor, on CME‐induced myocardial dysfunction are evaluated. Using a rat model of CME, we administrated glycyrrhizin in rats prior to CME induction. The level of HMGB1, TNF‐α, iNOS, IL‐6, IL‐1β, cleaved caspase‐3, Bax, and Bcl‐2 were measured. The serum level of cardiac troponin I, creatine kinase, was detected. The cardiac function and cardiomyocyte apoptosis were evaluated. The activation of TLR4/NF‐κB signaling pathway was analyzed. Glycyrrhizin prevented CME‐induced production of HMGB1, TNF‐α, iNOS, IL‐6, and IL‐1β. Glycyrrhizin inhibited CME‐induced cardiomyocyte apoptosis and the expression of cleaved caspase‐3 and Bax, while enhanced the expression of Bcl‐2. Glycyrrhizin decreased cardiac troponin I and creatine kinase levels and improved cardiac function. Glycyrrhizin prevented the activation of HMGB1/TLR4/NF‐κB signaling pathway. Glycyrrhizin ameliorated myocardial dysfunction in CME rats by preventing inflammation and apoptosis of cardiomyocytes.

This study aimed to exploit the potential therapeutic value of palmatine in treatment of cardiac hypertrophy and the underlying molecular mechanism. Rat hypertrophy model was established by intraperitoneal isoproterenol (ISO) injection. The hypertrophy was evaluated with cardiac hypertrophic parameters, hemodynamic parameters, lipid profile, and non-specific cardiac markers. The animals were intraperitoneally administrated with either palmatine or vehicle. The relative expressions of ANP, BNP, HDAC2, HDAC5, KLF4, and INPP5F transcripts were determined by real-time polymerase chain reaction (PCR). The relative protein levels of HDAC2, HDAC5, KLF4, and INPP5F were analyzed by immunoblotting. Palmatine treatment significantly attenuated ISO-induced hypertrophy in rats and elicited remarkable repressions in ANP, BNP, and HDAC2 transcriptions but not HDAC5. The downstream effector genes KLF4 and INPP5F were greatly restored in a dose-dependent manner in response to palmatine treatment. Our data demonstrated that palmatine possessed promising therapeutic potential against hypertrophy, which was mediated by modulation of HDAC2-KLF4/INPP5F pathway.