Objective To observe the effect of rosiglitazone on serum NOS/NO in apolipoprotein(apo) E knockout mice.Methods Twenty eight-week-old apoE knockout mice were intragastrically administrated 0.2 ml 5% sodium carboxymethycellulose for 12 weeks to establish the animal models of atherosclerosis,in which half of mice simultaneously received 10 mg?kg~(-1)?d~(-1) rosiglitazone as treatment.Ten wildtype mice were used as the normal control group.All mice were fed on normal chow diet.After 12 weeks,aorta were used for histomorphometric analysis by means of HE.Vessel blood was collected for plasma lipid,NO and NOS.Results Histomorphometric analysis showed that the area of atherosclerosis plaque in mice receiving rosiglitazone was significantly smaller than the mouse models of atherosclerosis,while the plasm lipid,NO and NOS were higher.Conclusion Rosiglitazone can inhibit the development of atherosclerosis,which mechanism is related to the protection of vascular endothelial function.

The antimicrobial peptide APKGVQGPNG (named YD), a natural peptide originating from Bacillus amyloliquefaciens CBSYD1, exhibited excellent antibacterial and antioxidant properties in vitro. These characteristics are closely related to inflammatory responses which is the central trigger for liver fibrosis. However, the therapeutic effects of YD against hepatic fibrosis and the underlying mechanisms are rarely studied. In this study, we show that YD improved liver function and inhibited the progression of liver fibrosis by measuring the serum transaminase activity and the expression of α-smooth muscle actin and collagen I in carbon tetrachloride-induced mice. Then we found that YD inhibited the level of miR-155, which plays an important role in inflammation and liver fibrosis. Bioinformatics analysis and luciferase reporter assay indicate that Casp12 is a new target of miR-155. We demonstrate that YD significantly decreases the contents of inflammatory cytokines and suppresses the NF-κB signaling pathway. Further studies show that transfection of the miR-155 mimic in RAW264.7 cells partially reversed the YD-mediated CASP12 upregulation, the downregulated levels of inflammatory cytokines, and the inactivation of the NF-κB pathways. Collectively, our study indicates that YD reduces inflammation through the miR-155–Casp12–NF-κB axis during liver fibrosis and provides a promising therapeutic candidate for hepatic fibrosis.