摘要
目的观察二苯乙烯苷(TSG)对ox-LDL诱导的U937细胞ICAM-1、VCAM-1及VEGF表达的影响,探讨TSG抗动脉粥样硬化(AS)的可能机制。方法体外培养经PMA处理过的U937细胞,在给予ox-LDL刺激的同时给予不同浓度TSG干预,采用黄嘌呤氧化酶法测定细胞培养液中SOD活力,TBA法测定培养液中MDA含量,蛋白免疫印迹法分析观察各组细胞ICAM-1、VCAM-1及VEGF的蛋白表达,逆转录聚合酶链反应法分析观察各组细胞ICAM-1和VCAM-1的基因表达。结果模型组细胞液总SOD活力较对照组明显降低,TSG高剂量及阳性对照组总SOD活力较模型组明显升高(P<0.05);模型组细胞液MDA水平较对照组明显升高,TSG高中剂量及阳性对照组较模型组明显升高(P<0.05)。蛋白免疫印迹分析显示,模型组ICAM-1、VCAM-1及VEGF的蛋白表达较对照组明显升高(P<0.05);TSG高剂量和辛伐他汀能明显降低ICAM-1、VCAM-1及VEGF表达(P<0.05)。逆转录聚合酶链反应分析显示,模型组细胞ICAM-1、VCAM-1 mRNA水平较正常组明显升高(P<0.01);TSG高剂量和辛伐他汀较模型组能明显降低ICAM-1、VCAM-1mRNA水平(P<0.01)。结论TSG具有抗氧化、抑制单核巨噬细胞黏附分子分泌作用;其作用可能与其抗动脉粥样硬化有关。
Aim To observe the effects of 2,3,4′, 5-tetrahydroxystilbene-2-0-β-D glucoside on expression of ICAM-1, VCAM-1 and VEGF excited by ox-LDL in U937 cell. Methods Differentiated U937 cells were cultured in vitro, excited by ox-LDL and intervened by different concentrations of TSG, then the level of SOD and MDA were determined. ICAM-1, VCAM-1 and VEGF protein were determined by Western blot and ICAM-1 mRNA and VCAM-1 mRNA were measured by reverse transcriptase-polymerase chain reaction （RT- PCR）. Results In comparison with those of the con- trol, the level of SOD remarkably decreased and the level of MDA remarkably increased in model group; the level of SOD increased markedly and the level of MDA decreased markedly in Simvastatin group and TSG 120 mg · L^-1 group（P 〈0.05）. Compared with that of the control, the expression of mRNA and pro- tein of ICAM-1 and VCAM-1 significantly increased, and the expression of protein of VEGF in model group significantly increased in model group （ P 〈 0. 05 ） ; the expression of mRNA and protein of ICAM-1 and VCAM-1, and the expression of VEGF protein were re- duced markedly in Simvastatin group and TSG 120 mg · L^- 1 group （ P 〈 0. 05 ）. Conclusion The TSG had anti-oxydation effect and inhibited the excretion of ad- hesion molecules in macrophage
出处
《中国药理学通报》
CAS
CSCD
北大核心
2008年第5期667-672,共6页
Chinese Pharmacological Bulletin
基金
江苏省南通科技创新计划资助项目(NoA4031)
江苏省南通社会发展计划资助项目(NoS40054)
