冠心康对气虚痰瘀证动脉粥样硬化大鼠炎症相关因子的影响

Influence of “Guan Xin Kang”on Inflammation-Related Factors in Rats with Atherosclerosis of Qi Deficiency and Phlegm-Blood Stasis

目的:探讨冠心康对气虚痰瘀证动脉粥样硬化大鼠炎症相关因子的调控作用。方法:将30只SD大鼠随机分为正常组、模型组和治疗组,每组10只;正常组和模型组大鼠予以生理盐水灌胃,治疗组给予冠心康灌胃治疗,疗程30 d。运用HE染色观察主动脉病理变化,全自动生化仪检测血清血脂水平,采用ELISA法检测血清C-反应蛋白(CRP)、黏附因子(ICAM-1)、白介素(IL-1、IL-6、IL-10)水平。结果:1治疗组大鼠主动脉粥样硬化程度较模型组减轻。2与正常组比较,模型组和治疗组大鼠血清TC和LDL-C水平显著增高(P<0.01);与模型组比较,治疗组大鼠血清TC、LDL-C水平显著下降(P<0.05)。3与正常组比较,模型组大鼠血清CRP、TNF-α、ICAM-1、IL-1β和IL-6水平显著升高(P<0.05,P<0.01);与模型组比较,治疗组大鼠血清CRP和ICAM-1水平显著下降(P<0.05)。结论:冠心康可减轻大鼠气虚痰瘀证动脉粥样硬化,其机制与调控炎症相关因子有关。

Objective ： To investigate the regulatory effect of ＂Guan Xin Kang＂ on inflammation-related factors in rats with atherosclerosis of qi deficiency and phlegm-blood stasis. Methods： Thirty SD rats were randomized into three groups： normal group, model group and treatment group, 10 rats in each group. Normal group and model group were given physiological saline, and the treatment group was given intragastric administration of ＂ Guan Xin Kang＂, with a course of 30 days. HE staining was employed to observe the pathological change of aorta; blood lipid in serum was assayed by automatic biochemistry analyzer; and ELISA assay was used to detect the levels of serum C-reactive protein （CRP） , cell adhesion factor（ ICAM-1 ） , interleukin （IL-1, IL-6, IL-10）. Results： 1The physiological changes of atheroselerosis were milder in the treatment group than in model group. 2Compared with the normal group, the levels of TC and LDL-C were significantly increased in the model group and treatment group （ P 〈 0, 01 ） ; compared with the model group, the levels of serum TC and LDL- C were decreased in the treatment group （P 〈0.05）. 3Compared with the normal group, the levels of serum CRP, TNF-α, ICAM-1, IL-1β and IL-6 were significantly increased in the model group（P 〈0.05, P 〈0.01 ） ; compared with the model group, the levels of serum CRP and ICAM- 1 were significantly decreased in the treatment group（ P 〈 0.05 ）. Conclusion ： ＂Guan Xin Kang＂ can fight against atherosclerosis of qi deficiency and phlegm-blood stasis by regulating inflammation-related factors.