Objective To elucidate the mechanism of interferon-gamma (IFN-γ) to inhibit the restenosis after successful percutaneous transluminal angioplasty (PTA).Methods A rabbit vascular restenotic model was constructed and...Objective To elucidate the mechanism of interferon-gamma (IFN-γ) to inhibit the restenosis after successful percutaneous transluminal angioplasty (PTA).Methods A rabbit vascular restenotic model was constructed and the proliferation of intimal smooth muscle cells (SMCs) were observed by monitoring their expression of proliferating cell nuclear antigen (PCNA) and platelet-derived growth factor β chain mRNA (PDGF-β mRNA) at the indicated time points. Results IFN-γ could significantly inhibit the expression of PCNA by intimal SMCs one week after denudation, when counting 200 intimal cells for PCNA-positive reactions with an inhibitory rate of 88.50% (P<0.001). IFN-γ could downregulate in situ expression of PDGF-β mRNA by these cells as we calculated the average number of PDGF-β mRNA positive cells per square millimetre area at ×400 magnification with reduced rates of 86.85% in 1 week group (P<0.001), of 93.66% in 2 week group (P<0.001) and of 52.92% in 4 week group (0.02<P<0.05), respectively. Conclusions The local production of PDGF-β by vascular intimal SMCs via an autocrine mechanism may be responsible for continuous proliferation of these cells and the formation of neointima after injury. This could be inhibited by IFN-γ through downregulating the expression of PDGF-β mRNA. These results provide an in vivo basis for IFN-γ to be used clinically for the management of restenosis after percutaneous transluminal angioplasty.展开更多
Objective: To study the antifibrotic effects of genistein(GE) and quercetin(QU) on rat hepatic stellate HSC-T6 cell proliferation stimulated with platelet-derived growth factor (PDGF), collagen synthesis and type I pr...Objective: To study the antifibrotic effects of genistein(GE) and quercetin(QU) on rat hepatic stellate HSC-T6 cell proliferation stimulated with platelet-derived growth factor (PDGF), collagen synthesis and type I procollagen messenger RNA (mRNA) expression stimulated with transforming growth factor b1 (TGFb1). Methods: Cell proliferation was measured by crystal violet staining assay. Collagen synthesis was determined by 3H-proline incorporation assay. Type I procollagen mRNA level was determined by reverse transcription polymerase chain reaction (RT-PCR). Results: GE (25~70 mmolL-1) and QU (6.25~50 mmolL-1) concentration-dependently attenuated PDGF-driven HSC-T6 cell proliferative activity. TGFb1-stimulated collagen synthesis was also reduced. This was associated with a decrease in type I procollagen mRNA expression, indicating an effect at a pretranslational level. Conclusion: GE and QU may have therapeutic potential against liver fibrosis by regulating PDGF and TGFb1 actions.展开更多
文摘Objective To elucidate the mechanism of interferon-gamma (IFN-γ) to inhibit the restenosis after successful percutaneous transluminal angioplasty (PTA).Methods A rabbit vascular restenotic model was constructed and the proliferation of intimal smooth muscle cells (SMCs) were observed by monitoring their expression of proliferating cell nuclear antigen (PCNA) and platelet-derived growth factor β chain mRNA (PDGF-β mRNA) at the indicated time points. Results IFN-γ could significantly inhibit the expression of PCNA by intimal SMCs one week after denudation, when counting 200 intimal cells for PCNA-positive reactions with an inhibitory rate of 88.50% (P<0.001). IFN-γ could downregulate in situ expression of PDGF-β mRNA by these cells as we calculated the average number of PDGF-β mRNA positive cells per square millimetre area at ×400 magnification with reduced rates of 86.85% in 1 week group (P<0.001), of 93.66% in 2 week group (P<0.001) and of 52.92% in 4 week group (0.02<P<0.05), respectively. Conclusions The local production of PDGF-β by vascular intimal SMCs via an autocrine mechanism may be responsible for continuous proliferation of these cells and the formation of neointima after injury. This could be inhibited by IFN-γ through downregulating the expression of PDGF-β mRNA. These results provide an in vivo basis for IFN-γ to be used clinically for the management of restenosis after percutaneous transluminal angioplasty.
基金Project supported by the National Natural Science Foundation of China No: 39670837
文摘Objective: To study the antifibrotic effects of genistein(GE) and quercetin(QU) on rat hepatic stellate HSC-T6 cell proliferation stimulated with platelet-derived growth factor (PDGF), collagen synthesis and type I procollagen messenger RNA (mRNA) expression stimulated with transforming growth factor b1 (TGFb1). Methods: Cell proliferation was measured by crystal violet staining assay. Collagen synthesis was determined by 3H-proline incorporation assay. Type I procollagen mRNA level was determined by reverse transcription polymerase chain reaction (RT-PCR). Results: GE (25~70 mmolL-1) and QU (6.25~50 mmolL-1) concentration-dependently attenuated PDGF-driven HSC-T6 cell proliferative activity. TGFb1-stimulated collagen synthesis was also reduced. This was associated with a decrease in type I procollagen mRNA expression, indicating an effect at a pretranslational level. Conclusion: GE and QU may have therapeutic potential against liver fibrosis by regulating PDGF and TGFb1 actions.
