Fang Wei, Zhang Hui-xin, Wang Lu-ya, Qin Yan-wen, Wu Ying, Wang Wei, Liu Bin
Department of Pathology, the Affiliated Hospital of the Capital Medical University of Beijing Anzhen Hospital, Beijing 100029, China.
Zhongguo Zhong Yao Za Zhi. 2007 Jul;32(13):1320-3.
To study the protecting effect of polygoni multiflori total glycosides (PMTG) on the atherosclerotic lesion formation and the expression of ICAM-1, VCAM-1 in aolipoprotein (apo) E-deficient transgenic mice.
Thirty-two female apoE-deficienct mice were randomized into four groups: PMTG high dose group (150 mg x kg x d), low dose group (25 mg x kg x d), atorvastatin positive control group (5 mg x kg x d), and model 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 (LDL-C) were measured by enzyme dynamics method. Transmission electron microscopy (TEM) were used to observe the morphologic changes of aortic endothelia cell. The expressions of NF-kappaB were studied by SABC immunohistochemistry.
As compared with the model control group. (1) PMTG could reduce the levels of serum TC, TG significantly (P < 0.01), and LDL-C level significantly (P < 0.01). (2) It could increase the levels of serum NO and the anti-oxidation capacities significantly (P < 0.01), but reduce the levels of serum MDA significantly (P < 0.01). (3) PMTG could keep the normal morphology of aortic endothelial cell. (4) PMTG could deregulated the expression of NF-kappaB in aortic wall.
PMTG could inhibit the occurrence and development of atherosclerotic lesions by its anti-oxidation abilities, which reduce LDL-C level. The low LDL-C level could deregulated the of expression of NF-kappaB, which could deregulated ICAM-1 and VCAM-1 in AopE-/-mice in aortic wall through.
研究何首乌总苷（PMTG）对载脂蛋白E基因缺陷转基因小鼠动脉粥样硬化病变形成及细胞间黏附分子-1（ICAM-1）、血管细胞黏附分子-1（VCAM-1）表达的保护作用。
将32只雌性载脂蛋白E基因缺陷小鼠随机分为四组：PMTG高剂量组（150mg·kg⁻¹·d⁻¹）、低剂量组（25mg·kg⁻¹·d⁻¹）、阿托伐他汀阳性对照组（5mg·kg⁻¹·d⁻¹）和模型组。在第10周结束时，处死所有小鼠。采用酶动力学法测定血清总胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白胆固醇（LDL-C）水平。用透射电子显微镜（TEM）观察主动脉内皮细胞的形态学变化。采用SABC免疫组织化学法研究核因子κB（NF-κB）的表达。
与模型对照组相比。（1）PMTG能显著降低血清TC、TG水平（P<0.01），显著降低LDL-C水平（P<0.01）。（2）能显著提高血清一氧化氮（NO）水平和抗氧化能力（P<0.01），但显著降低血清丙二醛（MDA）水平（P<0.01）。（3）PMTG能维持主动脉内皮细胞的正常形态。（4）PMTG能下调主动脉壁中NF-κB的表达。
PMTG可通过其抗氧化能力抑制动脉粥样硬化病变的发生发展，降低LDL-C水平。低LDL-C水平可下调NF-κB的表达，进而下调载脂蛋白E基因敲除（AopE-/-）小鼠主动脉壁中ICAM-1和VCAM-1的表达。
