摘要
目的:研究何首乌总苷(polygonum multiflorum total glycoside,PMTG)对载脂蛋白E基因缺陷(ApoE-/-)小鼠实验性动脉粥样硬化(atherosclerosis,AS)病变形成及细胞间黏附分子-1(intercellular adhesion molecule-1,ICAM-1)与血管细胞黏附分子-1(vascular cell adhesion molecule-1,VCAM-1)的表达影响,探讨何首乌总苷抑制AS病变形成的可能机制。方法:将ApoE-/-小鼠随机分为4组:何首乌总苷高剂量组(150 mg.kg-1.d-1)、低剂量组(25 mg.kg-1.d-1)、阿托伐他汀阳性药物组(5 mg.kg-1.d-1)及模型对照组。给药第10周后全部处死,检测4组血清脂质含量,一氧化氮(NO),总抗氧化能力(TAOC),丙二醛(MDA),主动脉AS粥样斑块面积及其与管腔面积的比值,主动脉壁ICAM-1及VCAM-1表达。结果:何首乌总苷高、低剂量组及阳性药物组与模型对照组ApoE-/-小鼠比较,显示:①何首乌总苷高、低剂量可以显著降低血清总胆固醇(TC),甘油三酯(TG)水平(P<0.01),升高高密度脂蛋白(HDL)水平(P<0.01);②明显增加血浆NO及TAC(P<0.05及P<0.01),减少MDA的生成(P<0.01);③何首乌总苷可减轻AS病变,减小斑块面积与管腔面积比值(P<0.05);④何首乌总苷可下调ICAM-1及VCAM-1的表达(P<0.01)。结论:何首乌总苷可能通过调节ApoE-/-小鼠血脂代谢、增强其抗氧化能力及下调主动脉壁ICAM-1及VCAM-1表达等上述环节的共同作用与影响,阻止ApoE-/-小鼠实验性动脉粥样硬化病变形成的发生、发展。
Objective： To study the effect of polygoni multiflori total glycosides （PMTG） on the expressions of ICAM-1 and VCAM-1 in the apoE-deficienct （ApoE-/-）mice with experimental atherosclerosis （AS） and underlying mechanism. Method： Thirty-two female apoE-deficienct mice were randomized into four groups： high dose PMTG group （ 150 mg·kg^-1·d^-1 ）, low dose PMTG group （25 mg·kg^-1·d^-1 ）, atorvastatin positive control group （5 mg·kg^-1·d^-1 ） and model group. At the end of the tenth week of treatment, all mice were killed. The serum levels of total cholesterol （TC）, triglyceride（TG）, high-density lipoprotein-cholesterol （HDL-C） were measured by enzyme dynamics method. Light microscopy were adopted to assess the degree of atherosclerotic plaque of aortic wall and image analysis was performed with computer. The expressions of ICAM-1 and VCAM-1 were studied by SABC imunohistochemistry. Result： In comparison with the model group, （1）PMTG reduced the levels of serum TC and TG significantly （ P 〈 0.01 ）, but elevated HDL level obviously （ P 〈 0,01 ）. （2） PMTG increased the levels of serum NO and the anti-oxidation capacities significantly （ P 〈 0.05 and P 〈 0.01）, but reduced the levels of serum MDA markedly （ P 〈0.01）. （3）PMTG reduced also the extent of atherosclerotic plaque of aorta areas were （P 〈0.05）. （4）PMTG deregulated the expres- sions of ICAM-1 and VCAM-1 in aortic wall. Conclusion： PMTG could inhibit the occurrence and development of atherosclerotic lesions by the regulating lipid metabolism and anti-oxidation and deregulating the of expressiona of ICAM-1 and VCAM-1 in AopE-/- mice in aortic wall.
出处
《中国中药杂志》
CAS
CSCD
北大核心
2005年第19期1542-1545,共4页
China Journal of Chinese Materia Medica
基金
国家教育部重点项目(105029)
