论文部分内容阅读
目的:观察sICAM-1、sCD40L与糖尿病大血管病变的关系,辛伐他汀干预后对sICAM-1、sCD40L水平变化和糖尿病大血管病变发生、发展的影响。方法:复制糖尿病合并大血管病变大鼠模型,随机分为正常对照组(A组)、正常干预组(B组)、糖尿病对照组(C组)、糖尿病干预组(D组),B组和D组给予辛伐他汀灌胃,A组和C组灌予相应量的生理盐水,8周末测四组血生化指标、血清sICAM-1和sCD40L,留取主动脉观察病理变化。结果:血糖C组和D组相近,均显著高于A组和B组(P<0.01);总胆固醇(TC)、甘油三酯(TG)及低密度脂蛋白(LDL-C)A组高于B组,C组高于D组;C组sICAM-1、sCD40L显著高于A组、B组和D组(P<0.01),D组明显低于C组(P<0.01);光镜下观察胸主动脉病变D组较C组减轻,A组与B组相比无明显变化。结论:sICAM-1、sCD40L与糖尿病大血管病变的发生有关;辛伐他汀干预治疗能够降低sICAM-1、sCD40L的水平,同时有明显延缓糖尿病大血管病变的作用。
Objective: To observe the relationship between sICAM-1, sCD40L and diabetic macroangiopathy and the effect of simvastatin on the changes of sICAM-1, sCD40L and the occurrence and development of diabetic macroangiopathy. Methods: A rat model of diabetic macroangiopathy was duplicated and randomly divided into normal control group (group A), normal control group (group B), diabetes control group (group C), diabetes intervention group (group D), group B The rats in group D were given simvastatin orally, and the rats in group A and group C were given the corresponding amount of saline. Blood biochemical indexes, serum sICAM-1 and sCD40L were measured at the end of the 8th week. The aorta was taken for observation of pathological changes. Results: The blood glucose in group C and group D were similar, which were significantly higher than those in group A and group B (P <0.01). The levels of total cholesterol (TC), triglyceride (TG) and low density lipoprotein (LDL-C) In group B, group C was higher than group D; sICAM-1 and sCD40L in group C were significantly higher than those in group A, group B and group D (P <0.01); Group D was significantly lower than group C (P <0.01) Under the observation of thoracic aorta lesions in group D than the C group, A group and B group compared with no significant change. Conclusion: sICAM-1 and sCD40L are associated with the development of macrovascular disease in diabetes mellitus. Simvastatin treatment can reduce the levels of sICAM-1 and sCD40L, at the same time significantly delay the progression of diabetic macroangiopathy.