| Summary: | 碩士 === 中國醫藥學院 === 醫學研究所 === 90 === There are approximately 250,000 people suffered from restenosis 6 months after percutaneous transluminal coronary angioplasty (PTCA) every year in the USA. One of the pathological mechanisms of restenosis has been attributed to abnormal proliferation of vascular smooth muscle cells. The aim of our study was to investigate the effect of Salvianolic B and Magnolol to inhibit proliferation of vascular smooth muscle cells and the mechanisms underlying the action of Salvianolic B and Magnolol. A10 cells, rat aortic smooth muscle cells,was used in this study to clarify these issues. From the in vitro result of western blot using antibody against PCNA and BrdU incorporation assay, we observed that 0.05mg/ml Magnolol significantly inhibit the proliferation of rat aortic smooth muscle cells. Whereas Magnolol demonstrated the inhibitory effects on BrdU incorporation in a dose-dependent manner; Salvianolic B did not show innibitory effect of vascular smooth muscle cells proliferation. In our study, we also evaluate the proteins that related to RIP and caspase-3 can be affected by Salvianolic B and Magnolol. It was found that the protein level of RIP and caspase-3 was significantly induced by Salvianolic B and Magnolol. On the other hand, Salvianolic B could inhibit the activity of NF-κB promoter. These results suggest that the proliferation of SMC can be regulated by Salvianolic B and Magnolol. Although PCNA protein level can be affectd by Magnolol, but we did not observe significant effect of Magnolol on P27 and RB protein expression level.
|
|---|
