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作 者:陈朝婷[1] 盛净[1] 汤政德[1] 陈祥华[1]
机构地区:[1]上海市交通大学医学院附属第九人民医院,上海200011
出 处:《中国新药与临床杂志》2007年第8期565-569,共5页Chinese Journal of New Drugs and Clinical Remedies
摘 要:目的:研究普伐他汀和阿司匹林对兔腹主动脉粥样硬化斑块CD40-CD40L表达及斑块稳定性的影响。方法:新西兰大白兔32只予高脂饲养16wk及腹主动脉球囊损伤术建立腹主动脉粥样硬化模型,分4组:P组(普伐他汀)、A组(阿司匹林)、A+P组(联合用药)与N组(不用药),分别予相应药物灌胃8wk。通过免疫组化检测比较各组兔腹主动脉粥样硬化斑块内CD40-CD40L表达、MMP-1、胶原及脂质含量变化,超声检测腹主动脉内膜-中膜厚度(IMT)改变,ELISA法测定血清C反应蛋白(CRP)变化,分析2药干预动脉粥样硬化斑块稳定性的机制。结果:用药各组兔腹主动脉斑块内CD40-CD40L表达较N组显著受抑,普伐他汀作用更显著(P组和A+P组均P<0.01);同时各用药组MMP-1的表达、IMT增厚及CRP增高较N组均得到明显抑制(P<0.01),P组和A+P组较N组斑块内脂质显著减少(P<0.01),胶原含量明显增加(P<0.01)。结论:普伐他汀和阿司匹林都可抑制斑块CD40-CD40L系统的表达,促进斑块的稳定性。普伐他汀促进斑块稳定的机制可能是多方面的。AIM: To study the effects of pravastatin and aspirin on the expression of CD40-CD40L and plaque stability. METHODS: A total of 32 New Zealand white rabbits were randomized into 4 groups after underwent balloon-induced arterial wall injury, then were given a diet of high lipid for 16 weeks followed by a high lipid diet for 1 week to establish atherosclerotic plaque model. Eight weeks after operation, rabbits were exposed to one of four treatments: no drug (N group), pravastatin (P group), aspirin (A group), combination of pravastatin and aspirin (A+P group). The expression of CD40-CD40L, MMP-1, content of collagen and lipid on plaque were measured by immunohistochemical staining, IMT was detected by ultrasound and the changes of serum CRP was tested with ELISA. RESULTS: The mechanism of drug intervention on plaque stability was analyzed. Compared with N group, the expression of CD40-CD40L on abdominal aorta plaque was significantly suppressed in other three groups, especially in P and A+P groups (P 〈 0.01). MMP-1 expression, IMT and CRP were decreased significantly (P 〈 0.01) in drug using groups. Lipid decreased and collagen increased significantly on plaque in P and A+P groups (P 〈 0.01). CONCLUSION: Both pravastatin and aspirin can inhibit the expression of CD40-CD40L on plaque and promote plaque stability. The mechanism of pravastatin promoting plaque stability may be multifactorial.
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