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目的:观察中药益脑康胶囊对动脉粥样硬化(AS)性急性脑缺血(AC)I大鼠组织中假性血友病因子(vWF)、血栓调节蛋白(TM)表达的影响。方法:将115只SD雄性大鼠随机分为6组,即正常对照组、益脑康预防组、AS模型组、AS加ACI模型组、益脑康治疗组、立普妥治疗组,采用腹腔注射维生素D3加高脂饲料喂养复制AS模型,并以内皮素-1注射法复制ACI模型。益脑康预防组在造模同时给予益脑康灌胃,其余各组大鼠在造模成功后分别予生理盐水、益脑康和立普妥灌胃治疗1周,在造模及治疗前后分别留取标本进行相关指标检测。结果:AS模型组和AS加ACI模型组大鼠脑组织可见vWF中等强度阳性、血管可见强阳性和非常强阳性表达。益脑康治疗组脑组织中为vWF弱阳性表达。在3个干预组血管中均表现为vWF中等强度阳性表达。AS造模组和ACI造模组大鼠脑组织可见TM中等强度阳性表达,而益脑康治疗组、立普妥治疗组脑组织观测到TM弱阳性表达。结论:预防性或治疗性使用益脑康胶囊能够增强TM表达,减弱vWF表达,可以减轻血管内皮损伤,纠正内皮功能紊乱,可延缓动脉粥样硬化和抗血栓形成。
Objective: To observe the effect of Yinaokang capsule on the expression of vWF and TM in the tissue of atherosclerotic (AS) acute cerebral ischemia (I) rats. Methods: One hundred and fifteen male Sprague-Dawley rats were randomly divided into 6 groups: normal control group, Yikangkang prophylaxis group, AS model group, AS plus ACI model group, YNKANG treatment group and Lipitor treatment group, The model of AS was replicated by injection of vitamin D3 and high fat diet, and the ACI model was replicated by endothelin - 1 injection. Yikangkang prevention group in the model while giving Yinaokang gavage, and the remaining groups of rats in the success of modeling were given saline, Yikang Kang and Lipitor gavage for 1 week before and after modeling and treatment Respectively specimens were taken for the detection of related indicators. Results: The expression of vWF in brain tissue of AS model group and AS plus ACI model group was moderately positive. The expression of VWF was strongly positive and strongly positive. Yiyukang treatment group was weakly positive for vWF in brain tissue. VWF was expressed as moderately positive in the three intervention groups. TM model group and ACI model group rats showed moderate TM positive expression of the brain, and Yinaokang treatment group, Lipitor treatment group brain tissue was observed TM weak positive expression. Conclusion: The prophylactic or therapeutic use of YNK can enhance the expression of TM and attenuate the expression of vWF, which can reduce the damage of vascular endothelial cells, correct the endothelial dysfunction and delay the development of atherosclerosis and antithrombosis.