暨南大学学报(自然科学与医学版)
暨南大學學報(自然科學與醫學版)
기남대학학보(자연과학여의학판)
JOURNAL OF JINAN UNIVERSITY(NATURAL SCIENCE & MEDICINE EDITION)
2013年
6期
588-592
,共5页
李平%甘剑挺%王正东%陈坚%梁祥文%刘明%尹瑞兴%黄锋
李平%甘劍挺%王正東%陳堅%樑祥文%劉明%尹瑞興%黃鋒
리평%감검정%왕정동%진견%량상문%류명%윤서흥%황봉
瑞舒伐他汀%血管平滑肌细胞%血小板衍生生长因子%增殖%迁移
瑞舒伐他汀%血管平滑肌細胞%血小闆衍生生長因子%增殖%遷移
서서벌타정%혈관평활기세포%혈소판연생생장인자%증식%천이
Rosuvastatin%vascular smooth muscle cells%platelet-derived growth factor%prolif-eration%migration
目的:探讨瑞舒伐他汀对血管平滑肌细胞增殖和迁移的影响及其分子机制。方法:采用血小板衍生生长因子(PDGF)-BB预处理血管平滑肌细胞,观察其对血管平滑肌细胞的增殖和迁移的作用,以及对基质金属蛋白酶(MMP)2、MMP9的表达、ERK1/2和P38蛋白的磷酸化水平的影响。结果:血小板衍生生长因子(PDGF)-BB处理后,血管平滑肌细胞的增殖和迁移明显上调,并伴随着细胞去分化为增殖型表型。而瑞舒伐他汀能显著抑制PDGF-BB诱导的血管平滑肌细胞的增殖、迁移以及表型转变;瑞舒伐他汀可抑制PDGF-BB诱导的血管平滑肌细胞中基质金属蛋白酶(MMP )2、MMP9的表达,并下调E RK1/2和P38蛋白的磷酸化水平。结论:瑞舒伐他汀可能通过部分下调PDGF-BB诱导的MAPK信号通路活性及MMP2、MMP9的表达,从而抑制血管平滑肌细胞的异常增殖和迁移,提示瑞舒伐他汀对内膜增生相关的动脉粥样硬化和介入后再狭窄具有治疗作用。
目的:探討瑞舒伐他汀對血管平滑肌細胞增殖和遷移的影響及其分子機製。方法:採用血小闆衍生生長因子(PDGF)-BB預處理血管平滑肌細胞,觀察其對血管平滑肌細胞的增殖和遷移的作用,以及對基質金屬蛋白酶(MMP)2、MMP9的錶達、ERK1/2和P38蛋白的燐痠化水平的影響。結果:血小闆衍生生長因子(PDGF)-BB處理後,血管平滑肌細胞的增殖和遷移明顯上調,併伴隨著細胞去分化為增殖型錶型。而瑞舒伐他汀能顯著抑製PDGF-BB誘導的血管平滑肌細胞的增殖、遷移以及錶型轉變;瑞舒伐他汀可抑製PDGF-BB誘導的血管平滑肌細胞中基質金屬蛋白酶(MMP )2、MMP9的錶達,併下調E RK1/2和P38蛋白的燐痠化水平。結論:瑞舒伐他汀可能通過部分下調PDGF-BB誘導的MAPK信號通路活性及MMP2、MMP9的錶達,從而抑製血管平滑肌細胞的異常增殖和遷移,提示瑞舒伐他汀對內膜增生相關的動脈粥樣硬化和介入後再狹窄具有治療作用。
목적:탐토서서벌타정대혈관평활기세포증식화천이적영향급기분자궤제。방법:채용혈소판연생생장인자(PDGF)-BB예처리혈관평활기세포,관찰기대혈관평활기세포적증식화천이적작용,이급대기질금속단백매(MMP)2、MMP9적표체、ERK1/2화P38단백적린산화수평적영향。결과:혈소판연생생장인자(PDGF)-BB처리후,혈관평활기세포적증식화천이명현상조,병반수착세포거분화위증식형표형。이서서벌타정능현저억제PDGF-BB유도적혈관평활기세포적증식、천이이급표형전변;서서벌타정가억제PDGF-BB유도적혈관평활기세포중기질금속단백매(MMP )2、MMP9적표체,병하조E RK1/2화P38단백적린산화수평。결론:서서벌타정가능통과부분하조PDGF-BB유도적MAPK신호통로활성급MMP2、MMP9적표체,종이억제혈관평활기세포적이상증식화천이,제시서서벌타정대내막증생상관적동맥죽양경화화개입후재협착구유치료작용。
Aim:To evalute the effect of rosuvastatin on the vascular smooth muscle proliferation and migration as well as the involved molecular mechanisms.Methods:Vascular smooth muscle was pretrea-ted with platelet-derived growth factor (PDGF)-BB.Then proliferation and migration of vascular smooth muscle cell,the protein expression of matrix metalloproteinase (MMP)2 and MMP9,as well as the phosphorylation levels of ERK1 /2 and P38 in vascular smooth muscle cells were observed.Results:This study showed that under the treatment of PDGF-BB,the proliferation and migration of vascular smooth muscle cell significantly increased,along with these cells differentiating into the proliferative phenotype. However,rosuvastatin significantly inhibited PDGF-BB-induced vascular smooth muscle cell prolifera-tion,migration,and the phenotypic change mentioned above.Further studies showed that rosuvastatin in-hibited PDGF-BB-induced the protein expression of matrix metalloproteinase (MMP)2 and MMP9,as well as the phosphorylation levels of ERK1 /2 and P38 in vascular smooth muscle cells.Conclusion:It suggested that rosuvastatin inhibited PDGF-BB-induced vascular smooth muscle cell proliferation and mi-gration,probably through downregulating the activity of MAPK signaling pathway and the protein expres-sion of MMP2 and MMP9 ,indicating that rosuvastatin may have therapeutic effects on atherosclerosis and restenosis after intervention,which are associated with intimal hyperplasia.