OBJECTIVES: To investigate the molecular mechanism by which salvianolic acid B (Sal-B) modulates mitochondrial functional homeostasis and alleviates myocardial ischemia-reperfusion (I/R) injury in mice. METHODS: Mouse cardiomyocyte HL-1 cells were pretreated with 5 μmol/L Sal-B with or without sh-Sirt1 transfection before exposure to hypoxia-reoxygenation (HR), and the changes in ATP production, mitochondrial superoxide activity, substrate oxidation level were evaluated. In the animal experiment, 36 C57BL/6J mice were randomized into 3 groups (n=12) for sham operation or ligation of the left anterior coronary artery to induce myocardial I/R injury with or without intravenous injection of Sal-B+I/R (50 mg/kg). In the rescue experiment, 60 adult C57BL/6J mice were randomized into 5 groups (n=12): sham-operated group, myocardial I/R group, Sal-B+I/R group, I/R+Sal-B+Sirt1fl/fl group, and I/R+Sal-B+cKO-Sirt1 group. Myocardial injury was evaluated with HE staining, and cardiac function was assessed by measurement of the ejection fraction and fractional shortening using echocardiography. RESULTS: In HL-1 cells with HR injury, Sal-B pretreatment significantly increased cellular ATP production, reduced mitochondrial superoxide anion levels, and enhanced oxygen consumption level. In the mouse models of myocardial I/R injury, Sal-B pretreatment markedly ameliorated I/R-induced structural disarray of the cardiac myocytes and improved cardiac ejection. Cycloheximide chase with Western blotting and ubiquitination assays after Sirt1-IP showed that Sal-B significantly inhibited Sirt1 degradation in HL-1 cells. Sirt1 knock-down reversed Sal-B-induced increases in ATP production, reduction in superoxide, and elevation of OCR in HL-1 cells. Cardiomyocyte-specific Sirt1 knockout obviously reversed Sal-B-mediated improvement in cardiac ejection function and myocardial structure damage in mice with myocardial I/R injury. CONCLUSIONS Sal-B promotes mitochondrial functional homeostasis in cardiomyocytes with HR injury and improves cardiac function in mice after myocardial I/R by inhibiting Sirt1 protein degradation.
Animals ; Sirtuin 1/metabolism* ; Myocardial Reperfusion Injury/physiopathology* ; Mice, Inbred C57BL ; Mice ; Myocytes, Cardiac/drug effects* ; Benzofurans/pharmacology* ; Homeostasis/drug effects* ; Male ; Mitochondria/drug effects* ; Depsides

Objective To explore the bacteriostatic efficacy of snake venom antibacterial peptide OH-CATH and chitosan as ar-tificial implant coating on escherichia coli (E .coli) .Methods The catheters and dacron patches (blank group ,chitosan group ,cef-operazone group and antibacterial peptide group) were performed the pretreatment .Then the in vitro bacteriostatic test was conduc-ted to evaluate the antibacterial activity U value on E .coli ATCC 25922 and cephalosporin-resistant E .coli on 1 d and on 7 d after putting it into plasma .Results The cefoperazone group and the antibiotic peptide group had the very powerful antibacterial activity on E .coli ATCC 25922 on 1 ,7 d ,but the antibacterial activity of the cefoperazone group was stronger than that of the antibiotic peptide group(P<0 .05);the cefoperazone group had no antibacterial activity on cephalosporin-resistant E .coli ,but the antibiotic peptide group had significantly antibacterial activity on 1 ,7 d(P<0 .01) .Conclusion Snake venom antibacterial peptide OH-CATH has very obvious antibacterial effect on the standard strain and drug-resistant strain of E .coli and its value applied in artificial im-plant coating is affirmed .