title: [The effects of polygoni multiflori total glycosides on the experimentally atherosclerotic formation in apoE-deficient mice].
abstract: OBJECTIVE
  To study the effect of polygoni multiflori total glycosides (PMTG) on the expressions of ICAM-1 and VCAM-1 in the apoE-deficienct (ApoE-/-)mice with experimental atherosclerosis (AS) and underlying mechanism.
  
  
  METHODS
  Thirty-two female apoE-deficienct mice were randomized into four groups: high dose PMTG group (150 mg x kg(-1) x d(-1)), low dose PMTG group (25 mg x kg(-1) x d(-1)), atorvastatin positive control group (5 mg x kg(-1) x d(-1)) and model group. At the end of the tenth week of treatment, all mice were killed. The serum levels of total cholesterol (TC), triglyceride(TG), high-density lipoprotein-cholesterol (HDL-C) were measured by enzyme dynamics method. Light microscopy were adopted to assess the degree of atherosclerotic plaque of aortic wall and image analysis was performed with computer. The expressions of ICAM-1 and VCAM-1 were studied by SABC imunohistochemistry.
  
  
  RESULTS
  In comparison with the model group, (1) PMTG reduced the levels of serum TC and TG significantly (P < 0.01), but elevated HDL level obviously (P < 0.01) . (2) PMTG increased the levels of serum NO and the anti-oxidation capacities significantly (P < 0.05 and P < 0.01), but reduced the levels of serum MDA markedly (P < 0.01). (3) PMTG reduced also the extent of atherosclerotic plaque of aorta areas were (P < 0.05). (4) PMTG deregulated the expressions of ICAM-1 and VCAM-1 in aortic wall.
  
  
  CONCLUSIONS
  PMTG could inhibit the occurrence and development of atherosclerotic lesions by the regulating lipid metabolism and anti-oxidation and deregulating the of expressiona of ICAM-1 and VCAM-1 in AopE-/- mice in aortic wall.
authors.affiliation: Department of Pathology, Beijing Anzhen Hospital, Beijing 100029, China. wendyf3287@126.com
authors.forename: Wei
authors.initials: W
authors.lastname: Fang
authors.forename: Hui-Xin
authors.initials: HX
authors.lastname: Zhang
authors.forename: Lu-Ya
authors.initials: LY
authors.lastname: Wang
authors.forename: Ying
authors.initials: Y
authors.lastname: Wu
authors.forename: Yan-Wen
authors.initials: YW
authors.lastname: Qin
authors.forename: Wei
authors.initials: W
authors.lastname: Wang
authors.forename: Lan-Ping
authors.initials: LP
authors.lastname: Du
authors.forename: Bin
authors.initials: B
authors.lastname: Lu
mesh_terms: D000818:Animals; D001011:Aorta / Q000378:metabolism / Q000473:pathology; D001057:Apolipoproteins E / Q000172:deficiency*; D050197:Atherosclerosis / Q000378:metabolism* / Q000473:pathology; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D005260:Female; D006027:Glycosides / Q000302:isolation & purification / Q000494:pharmacology*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism*; D008315:Malondialdehyde / Q000097:blood; D051379:Mice; 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 / Q000378:metabolism*
chemical_list: D001057:Apolipoproteins E; D008076:Cholesterol, HDL; D006027:Glycosides; D014280:Triglycerides; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D009569:Nitric Oxide; D008315:Malondialdehyde; D002784:Cholesterol