何首乌总甙抑制动脉粥样硬化病变形成

的　研究何首乌总甙对载脂蛋白E基因缺陷小鼠实验性动脉粥样硬化病变形成的保护作用。方法　将载脂蛋白E基因缺陷小鼠随机分为4组:何首乌总甙高剂量组[15 0mg/ (kg·d) ]、低剂量组[2 5mg/ (kg·d) ]、阿托伐他汀阳性药物组[5mg/ (kg·d) ]及空白对照组,给药第10周后全部处死,酶法检测四组血清脂质含量,图象分析法测定主动脉粥样硬化斑块面积和管腔面积,计算斑块面积与管腔面积的比值。结果　(1)何首乌总甙高、低剂量组及阳性药物组总胆固醇分别为6 4 9.3±72 .2mg/dL、6 32 .6±5 5 .1mg/dL和4 97.4±14 0 .8mg/dL ,均显著低于空白对照组(80 9.4±4 2 .6mg/dL ,P <0 .0 1) ;甘油三酯分别为12 6 .6±4 8.1mg/dL、14 5 .6±37.9mg/dL和172 .1±15 .7mg/dL ,均显著降低于空白对照组(2 5 3.3±4 2 .6mg/dL ,P <0 .0 1) ;而高密度脂蛋白胆固醇分别为117.1±14 .9mg/dL、113.5±2 3.3mg/dL和12 6 .7±12 .8mg/dL ,均显著高于空白对照组(6 7.3±10 .6mg/dL ,P <0 .0 1) ;治疗组间无显著性差异(P >0 .0 5 )。(2 )何首乌总甙高剂量组、低剂量组及阳性药物组载脂蛋白E基因缺陷小鼠主动脉粥样硬化病变减轻且动脉粥样硬化斑块面积/管腔面积比值分别为3.97%±0 .6 2 %、3.11%±0 .0 1%和0 .86 %±0 .0 7% ,均小于空

The Inhibiting Effect of Polygonum Multiflorum Total Glycoside on the Atherosclerotic Lesion Formation

Aim To study the protecting effect of Polygoni Multiflori total glycosides(PMTG)on the atherosclerotic lesion formation. Methods Thirty-two female apolipoprotein E gene deficiency mice were randomized into four groups: PMTG high dose group [150 mg/(kg·d)],low dose group [25 mg/(kg·d)],atorvastatin positive control group [5 mg/(kg·d)],and blank control group. At the end of the tenth week, all mice were killed. The serum levels of total cholesterol (TC), Triglyceride (TG), high density lipoprotein cholesterol (HDLC)were measured by enzyme dynamics method. Light microscopy were adopted to assess the degree of As lesions of aortic wall and image analysis was performed with computer. Results As compared with the blank control group, 1.PMTG could reduce the levels of serum TC, TG significantly (TC: 649.3±72.2 mg/dL, 632.6±55.1 mg/dL, 497.4±140.8 mg/dL vs 809.4±42.6 mg/dL, respectively, p<0.01; TG: 126.6±48.1 mg/dL, 145.6±37.9 mg/dL, 172.1±15.7 mg/dL vs 253.3±42.6 mg/dL, respectively, p<0.01); but elevate HDLC level significantly(117.1±14.9 mg/dL, 113.5±23.3 mg/dL, 126.7±12.8 mg/dL vs 67.3±10.6 mg/dL, respectively, p<0.01). There are no differences beween cured groups in the serum level of blood lipids (p>0.05). 2.It could also reduce the extent of atherosclerotic lesion and the aorta plaque areas were significantly lower (3.97%±0.62%, 3.11%±0.01%, 0.86%±0.07% vs 18.50%±6.54%, respectively, p<0.05). Conclusion The resulting data provide the occurrence and the development of atherosclerotic lesions could be inhibited by the PMTG because of its lipid-regulated ability.