摘要
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 0 5和P <0 0 1)。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。
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.
出处
《北京中医药大学学报》
CAS
CSCD
北大核心
2004年第4期27-30,共4页
Journal of Beijing University of Traditional Chinese Medicine
基金
国家重点基础研究发展规划项目课题 (No G19990 5 44 0 5 )
