title: Panax notoginseng reduces atherosclerotic lesions in ApoE-deficient mice and inhibits TNF-alpha-induced endothelial adhesion molecule expression and monocyte adhesion.
abstract: It is widely recognized that atherogenesis is associated with vascular inflammation. Panax notoginseng , a commonly used herb in China, has been shown to possess anti-inflammatory activity. In the present study, the antiatherogenic effect of P. notoginseng saponins (PNS) was examined in apolipoprotein E (apoE)-deficient mice. The molecular mechanisms responsible for the antivascular inflammatory effect of PNS on human coronary artery endothelial cells (HCAECs) were also investigated in vitro. PNS, dissolved in drinking water, was administered orally to two treatment groups at dosages of 4.0 and 12.0 mg/day/mouse, respectively. After 8 weeks, atherosclerosis in the entire aortic area was assessed using an en face method. Compared with the control group, both low- and high-dose PNS-treated groups showed a significant decrease in extent of atherosclerotic lesions by 61.4 and 66.2%, respectively (P < 0.01). PNS also notably reduced serum lipid levels. Serum levels of IL-6 and TNF-alpha in all groups of apoE-deficient mice were below the detection limit. In vitro studies showed that PNS dose-dependently inhibited monocyte adhesion on activated endothelium, as well as the expression of TNF-alpha-induced endothelial adhesion molecules, such as ICAM-1 and VCAM-1. In conclusion, PNS has antiatherogenic activity through, at least in part, its lipid-lowering and antivascular inflammatory mechanisms.
authors.affiliation: Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.
authors.forename: Jian-Bo
authors.initials: JB
authors.lastname: Wan
authors.forename: Simon Ming-Yuen
authors.initials: SM
authors.lastname: Lee
authors.forename: Jing-Dong
authors.initials: JD
authors.lastname: Wang
authors.forename: Nan
authors.initials: N
authors.lastname: Wang
authors.forename: Cheng-Wei
authors.initials: CW
authors.lastname: He
authors.forename: Yi-Tao
authors.initials: YT
authors.lastname: Wang
authors.forename: Jing X
authors.initials: JX
authors.lastname: Kang
mesh_terms: D000818:Animals; D001057:Apolipoproteins E / Q000172:deficiency* / Q000235:genetics; D050197:Atherosclerosis / Q000188:drug therapy* / Q000235:genetics / Q000276:immunology; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000235:genetics* / Q000276:immunology; D002478:Cells, Cultured; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000187:drug effects; D042783:Endothelial Cells / Q000187:drug effects / Q000276:immunology; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009000:Monocytes / Q000276:immunology; D053723:Panax notoginseng / Q000737:chemistry*; D010936:Plant Extracts / Q000008:administration & dosage* / Q000737:chemistry; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology*
chemical_list: D001057:Apolipoproteins E; D015815:Cell Adhesion Molecules; D010936:Plant Extracts; D014409:Tumor Necrosis Factor-alpha