气血并治方及方中理气药、活血药对高脂血症血瘀大鼠炎症因子的干预作用

目的探讨动脉粥样硬化初期炎症反应机制和气血并治复方及方中理气药、活血药对其干预作用.方法采用高脂应激造成大鼠高脂血症血瘀模型,观察各组大鼠脂质代谢、白介素-6、白介素-8和白细胞粘附活化分子表达率(CD11b)的变化. 结果和模型组比较,全方组对TC、TG、TC/HDL-C、LDL-C、IL-6、wCD11b和zCD11b有显著降低作用,理气药组对TC、TG、LDL-C、IL-6、IL-8和wCD11b有显著降低作用,活血药组对TC、LDL-C、IL-6和wCD11b有显著降低作用(P<0.05和P<0.01).结论气血并治方可干预AS炎症反应,是抗AS的作用机制之一,方中理气药和活血药作用机制不尽相同,有协同作用.

Intervening Effects of Qixuebingzhi Formula and Qi-Regulating and Blood-Activating Drugs in the Formula on the Inflammatory Factors in the Rat with Hyperlipidemia/Blood Stagnation

Objective To investigate the mechanism of the early inflammatory reaction in atherosclerosis (AS) and to observe the intervening effects of Qixuebingzhi Formula (QF) and qi-regulating and blood-activating drugs in QF. Method The rat model of hyperlipidemia/blood stagnation was established by using a high-lipid stressor. The changes in the lipid metabolism,levels of IL-6 and IL-8,and the expression rate of the activated-leukocyte cell adhesion molecules were observed. Results Compared with those in the model group,the levels of TC,TG,TC/HDL-C,LDL-C,IL-6,wCD11b,and zCD11b were markedly decreased in the QF-group;the levels of TC,TG,LDL-C,IL-6,IL-8,and wCD11b were markedly decreased in the qi-regulating drug group;and the levels of TC,LDL-C,IL-6,and wCD11b were markedly decreased in the blood-activating drug group ( P <0.05 and P <0.01,respectively). Conclusion QF may interfere with the inflammatory reaction of AS,which is one of the mechanisms by which QF resists AS. Although the mechanisms of the effects of qi-regulating and blood-activating drugs in QF are not totally same,the two kinds of drugs exert a cooperative effect.