[PMTG对载脂蛋白E基因缺陷小鼠动脉粥样硬化病变形成及细胞间黏附分子-1和血管细胞黏附分子-1表达的影响]

[Effect of PMTG on atherosclerotic lesion formation and expression of ICAM-1 and VCAM-1 in ApoE-deficient mice].

作者信息

Fang Wei, Zhang Hui-xin, Wang Lu-ya, Qin Yan-wen, Wu Ying, Wang Wei, Liu Bin

机构信息

Department of Pathology, the Affiliated Hospital of the Capital Medical University of Beijing Anzhen Hospital, Beijing 100029, China.

出版信息

Zhongguo Zhong Yao Za Zhi. 2007 Jul;32(13):1320-3.

PMID:17879736

Abstract

OBJECTIVE

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.

METHOD

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.

RESULT

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.

CONCLUSION

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.

摘要

目的

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。

方法

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。

结果

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。