第一军医大学学报
第一軍醫大學學報
제일군의대학학보
JOURNAL OF FIRST MILITARY MEDICAL UNIVERSITY
2004年
3期
247-251
,共5页
欧阳平%彭文烈%许顶立%赖文岩%徐安龙
歐暘平%彭文烈%許頂立%賴文巖%徐安龍
구양평%팽문렬%허정립%뢰문암%서안룡
血管平滑肌细胞%绿茶多酚%晚期糖基化终产物%细胞增殖%丝裂素活化蛋白激酶
血管平滑肌細胞%綠茶多酚%晚期糖基化終產物%細胞增殖%絲裂素活化蛋白激酶
혈관평활기세포%록다다분%만기당기화종산물%세포증식%사렬소활화단백격매
tea polyphenols%muscle,smooth,vascular drug effects%advanced glycation end products%cell proliferation%mitogen-activated protein kinase
目的本研究观察绿茶多酚对晚期糖基化终产物(AGEs)刺激下离体大鼠胸主动脉血管平滑肌细胞增殖的影响.方法体外培养大鼠主动脉血管平滑肌细胞(VSMCs)应用不同浓度的AGEs分别刺激VSMCs并设立对照组进行比较,将不同剂量的绿茶多酚与AGEs共同作用并设立对照组进行比较,采用非放射性的MTS/PES法确定血管平滑肌细胞的增殖状态.结果与对照组相比,晚期糖基化终产物对血管平滑肌细胞增殖具有明显的刺激作用.在晚期糖基化终产物刺激下,绿茶多酚可明显抑制血管平滑肌细胞的生长.AGEs对p44/42 MAPK磷酸化蛋白表达有显著的增强作用,此作用可被绿茶多酚抑制.结论本研究提示绿茶多酚可抑制晚期糖基化终产物诱导的血管平滑肌细胞增殖及p44/p42MAPK磷酸化蛋白的表达.
目的本研究觀察綠茶多酚對晚期糖基化終產物(AGEs)刺激下離體大鼠胸主動脈血管平滑肌細胞增殖的影響.方法體外培養大鼠主動脈血管平滑肌細胞(VSMCs)應用不同濃度的AGEs分彆刺激VSMCs併設立對照組進行比較,將不同劑量的綠茶多酚與AGEs共同作用併設立對照組進行比較,採用非放射性的MTS/PES法確定血管平滑肌細胞的增殖狀態.結果與對照組相比,晚期糖基化終產物對血管平滑肌細胞增殖具有明顯的刺激作用.在晚期糖基化終產物刺激下,綠茶多酚可明顯抑製血管平滑肌細胞的生長.AGEs對p44/42 MAPK燐痠化蛋白錶達有顯著的增彊作用,此作用可被綠茶多酚抑製.結論本研究提示綠茶多酚可抑製晚期糖基化終產物誘導的血管平滑肌細胞增殖及p44/p42MAPK燐痠化蛋白的錶達.
목적본연구관찰록다다분대만기당기화종산물(AGEs)자격하리체대서흉주동맥혈관평활기세포증식적영향.방법체외배양대서주동맥혈관평활기세포(VSMCs)응용불동농도적AGEs분별자격VSMCs병설립대조조진행비교,장불동제량적록다다분여AGEs공동작용병설립대조조진행비교,채용비방사성적MTS/PES법학정혈관평활기세포적증식상태.결과여대조조상비,만기당기화종산물대혈관평활기세포증식구유명현적자격작용.재만기당기화종산물자격하,록다다분가명현억제혈관평활기세포적생장.AGEs대p44/42 MAPK린산화단백표체유현저적증강작용,차작용가피록다다분억제.결론본연구제시록다다분가억제만기당기화종산물유도적혈관평활기세포증식급p44/p42MAPK린산화단백적표체.
Objective To determine the effects of green tea polyphenols(GTP) on advanced glycation end products (AGEs)-induced proliferation and expression ofp44/42 mitogen-activated protein kinase (MAPK) of rat vascular smooth muscle cells (VSMCs). Methods Rat aortic VSMCs isolated and culturedin vitro were stimulated with AGEs in the presence or absence of GTP at different concentrations, followed by quantitative analysis of the cell proliferation with colorimetric assay. The p44/42 MAPK activity was evaluated by immunoblotting technique using anti-p44/42 phospho-MAPK antibody. Results Compared with the control cells(without GTP treatment), GTP dose-dependently inhibited AGE-stimulated VSMC proliferation (P<0.05), and the p44/42 MAPK activity was significantly enhanced. The effects of AGEs were antagonized by GTP (372±41 vs 761±56, P<0.05). Conclusion GTP can inhibit the AGE-induced proliferation and p44/42 MAPK expression of rat VSMCs.