Influence of Rivaroxaban on Vascular Endothelial Function and p38MAPK/NF-κB Pathway in Rats with Lower Extremity Arteriosclerosis Obliterans / 中国药师

Objective:To explore the influence of rivaroxaban on vascular endothelial function and p38MAPK/NF-κB pathway in the rats with arteriosclerosis obliterans. Methods:The rats were divided into the sham operation group,the model group,rivaroxaban low dose group,rivaroxaban medium dose group and rivaroxaban high dose group. The contents of nitric oxide (NO) and endothelin (ET-1) in serum were detected, the number of endothelial cells in serum was studied, and the expression level of p38MAPK, p-p38MAPK and NF-κB were measured. Results:Compared with that of the model group, the number of endothelial cells in venous blood of rivaroxaban groups decreased. The content of NO in serum of rivaroxaban groups was significantly higher than that of the model group,and the content of ET-1 was significantly lower than that of the model group(P<0.05). The expression level of p-p38MAPK in arterial vessels of rivaroxaban groups was significantly lower than that of the model group,and the expression level of NF-κB was sig-nificantly higher than that of the model group(P<0.05),and the effects were all in a dose-dependent manner. Conclusion:Rivarox-aban can improve vascular endothelial function in the rats with arteriosclerosis obliterans,and the effects may be achieved by modula-ting the p38MAPK / NF-κB pathway.

Rosiglitazone inhibits osteoclastogenesis in rheumatoid arthritis by down-regulating RANKL expression and suppressing ERK phosphorylation / 中国病理生理杂志

AIM: To investigate the effects of rosiglitazone on fibroblast-like synoviocyte ( FLS )-induced osteoclastogenesis in rheumatoid arthritis ( RA) and the related mechanism.METHODS: RA-FLS were cocultured with peripheral blood monocytes from healthy volunteers in the presence of macrophage colony-stimulating factor ( M-CSF) and rosiglitazone.Osteoclasts were assayed by tartrate-resistant acid phosphatase ( TRAP) staining.Resorption lacunae area was identified by toluidine blue staining and quantified by image analysis software.The mRNA expression of RANKL and OPG was evaluated by real-time PCR, and the protein levels of RANKL, OPG, p-ERK, p-p38 and p-JNK were measured by Western blot.RESULTS:Compared with control group ( without rosiglitazone treatment) , rosiglitazone at concentration of 15 μmol/L significantly decreased the number of osteoclasts (P0.05 ) . CONCLUSION:Rosiglitazone inhibits RA-FLS-induced osteoclast formation and its resorption activity by down-regulating RANKL expression and ERK phosphorylation, suggesting that rosiglitazone may inhibit RA osteoclastogenesis and bone re-sorption.