水蛭素对动脉内皮保护作用的实验研究

The Protective Effects of Hirudo on Arterial Endothelium

目的:探讨水蛭保护动脉粥样硬化动脉内皮的作用及可能机制。方法:55只大耳白兔随机分为2组。正常对照组(A组)予普通喂养,模型组予高脂喂养9周。确定模型成功后模型组再次分为未处理组(B组)继续高脂喂养;低剂量水蛭组(C组)加用水蛭粉0.5g/(kg·d);高剂量水蛭组(D组)加用水蛭粉1.5g/(kg·d);阿托伐他汀组(E组)加用阿托伐他汀2.5mg/(kg·d)。继续喂养8周后比较各组的胸主动脉大体形态、组织形态差异和血清总胆固醇(TC)、低密度脂蛋白(LDL)、一氧化氮(NO)、内皮素(ET)-1、前列环素(PG)F-1-α、血栓烷(TX)B2及C-反应蛋白(CRP)等指标差异。结果:B、C、D、E组平均斑块面积分别为74%、45%、21%、20%。D组TC、TXB2、ET-1、CRP低于B组,NO、PGF-1-α显著高于B组,TC、LDL、NO高于E组,ET-1低于E组,差异有统计学意义(均P<0.05)。结论:水蛭可能通过升高NO、PGF-1-α,抑制TXB2、ET-1及炎症反应来保护动脉内皮。

Objective： To investigate the role and possible mechanism of hirudo on the vascular endothelium in atherosclerosis. Methods： Fifty-five rabbits were randomly divided into control group （A） fed the normal diet and model group fed with high-fat diet for 9 weeks. After determining the success of the model, rabbits of model group were sub- divided into B group fed with high-fat diet, C group fed with high-fat diet and mixed low dose of hirudo medicinalis powder 0.5 g/（kg· d）, D group fed high-fat diet and high dose of hirudo medicinalis powder 1.5 g/（kg· d） and E group fed with high-fat diet and atorvastatin 2.5 mg/（kg· d）. At the end of 8-week, the morphological figures of thoracic aortas, serum levels of total cholesterol （TC）, low-density lipoprotein （LDL）, blood fat, nitric oxide （NO）, endothelin （ET）-1, prostacyclin （PG） F-l-α, thromboxane （TX） B2 and C-reactive protein （CRP） were compared between groups. Results： The average plaque areas were 74%, 45%, 21% and 20% in B, C, D and E groups respectively. Values of TC, TXB2, ET-1 and CRP were significantly lower in D group than those of B group （P 〈 0.05）. Values of NO and PGF-1α were significantly higher in D group than those of B group （P 〈 0.05）. Levels of TC, LDL and NO were significantly higher in D group than those of E group （P 〈 0.05）, while the level of ET-1 was significantly lower in D group than that of E group （P 〈 0.05）. Conclusion： Hirudo has a remarkable protective effect on the vascular endothelium by increasing NO and PG F-l-α nd inhibiting TXB2, ET-1 and inflammatory reaction.