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作 者:常宏[1] 赵明镜[1] 雷环[1] 赵一舟[1] 吕晞滢[1] 赵保胜[2] 杨瑞薛
机构地区:[1]北京中医药大学东直门医院中医内科学教育部重点实验室中医内科学北京市重点实验室,北京100700 [2]北京中医药大学,北京100029
出 处:《辽宁中医杂志》2015年第1期193-196,I0001,共5页Liaoning Journal of Traditional Chinese Medicine
基 金:国家自然科学基金面上项目(81173234)
摘 要:目的:观察益气活血解毒方对血管损伤后血管重构指标及炎性因子的干预作用。方法:采用球囊导管损伤大鼠左侧颈总动脉模型,动物随机分为假手术组、模型组、他汀组和益气活血解毒组。用药后7天行HE染色,观察血管壁各层面积和管腔内径,放免法检测血清单核细胞趋化因子-1(MCP-1)、C反应蛋白(CRP)以及转化生长因子-β(TGF-β)的浓度。结果:与假手术组比,模型组内膜轻度增生(P<0.01),外膜明显增厚,面积变大(P<0.05),MCP-1、CRP、TGF-β含量显著升高(P<0.01);与模型组比,益气活血解毒方明显减少内膜面积(P<0.05),降低CRP、TGF-β的含量(P<0.01);阿托伐他汀显著降低TGF-β的含量(P<0.05)。结论:球囊损伤大鼠颈总动脉早期,外膜增生明显,内膜有轻度增生,但管腔内径无显著变化,血管重构主要表现为正性重构,并伴随MCP-1、CRP、TGF-β含量的显著上升。益气活血解毒方抑制新生内膜生成,可能与降低CRP、TGF-β的含量有关。Objective: To observe the effect of Yiqi Huoxue Jiedu Recipe on vascular remodeling and inflammatory factors in injured vessels. Methods: Models of the left common carotid artery balloon injury in rats was used and rats were randomly divided into model group,atorvastatin group and Yiqihuoxuejie group,with sham group as the control. Seven days later,by using HE staining we observed the area of the vascular wall and lumen diameter. The concentrations of MCP-1,CRP and TGF-β were tested by radioimmunoassay. Results: Compared with sham group,the intima hyperplasia was slight( P〈0. 01),adventitial area became larger( P〈0. 05) and the concentrations of MCP-1,CRP and TGF-β increased significantly( P〈0. 01) in model group. Compared with model group,Yiqi Huoxue Jiedu Recipe could obviously reduce the intimal area( P〈0. 05) and decrease CRP and TGF-β remarkably( P〈0. 01). Atorvastatin lessened TGF-β significantly( P〈0. 05). Conclusion: Vascular remodeling mainly represents the positive remodeling,including adventitial thickening and intimal hyperplasia. There is no significant change in the lumen diameter,accompanied by remarkable increase of concentrations of MCP-1,CRP and TGF-β in the early stage of common carotid artery balloon injury in rats. Yiqi Huoxue Jiedu Recipe inhibits intimal hyperplasia which may be associated with the reduction of the concentrations of CRP and TGF-β.
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