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


METHODS
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.


RESULTS
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.


CONCLUSIONS
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.
Fang
Wei
W
Department of Pathology, the Affiliated Hospital of the Capital Medical University of Beijing Anzhen Hospital, Beijing 100029, China. wendyf3287@126.com
Zhang
Hui-xin
HX
Wang
Lu-ya
LY
Qin
Yan-wen
YW
Wu
Ying
Y
Wang
Wei
W
Liu
Bin
B
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001013:Aorta, Thoracic / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D001057:Apolipoproteins E / Q000172:deficiency* / Q000235:genetics; D050197:Atherosclerosis / Q000097:blood / Q000473:pathology / Q000517:prevention & control*; D002784:Cholesterol / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D042783:Endothelial Cells / Q000187:drug effects / Q000473:pathology / Q000648:ultrastructure; D005260:Female; D006027:Glycosides / Q000302:isolation & purification / Q000494:pharmacology*; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis*; D008315:Malondialdehyde / Q000097:blood; D051379:Mice; D018345:Mice, Knockout; D046529:Microscopy, Electron, Transmission; D016328:NF-kappa B / Q000378:metabolism; D009569:Nitric Oxide / Q000097:blood; D010946:Plants, Medicinal / Q000737:chemistry; D028502:Polygonum / Q000737:chemistry*; D011897:Random Allocation; D014280:Triglycerides / Q000097:blood; D019010:Vascular Cell Adhesion Molecule-1 / Q000096:biosynthesis*
D000975:Antioxidants; D001057:Apolipoproteins E; D008078:Cholesterol, LDL; D006027:Glycosides; D016328:NF-kappa B; D014280:Triglycerides; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D009569:Nitric Oxide; D008315:Malondialdehyde; D002784:Cholesterol