title: The anti-atherosclerotic effect of olive leaf extract is related to suppressed inflammatory response in rabbits with experimental atherosclerosis.
abstract: BACKGROUND
  The anti-atherogenic effect of olive leaf extract is supposed to be related to its activities of anti-oxidation and anti-inflammation.
  
  
  OBJECTIVE
  To prove the effect of anti-atherosclerosis by olive leaf extract (OLE) and to elucidate the mechanism behind.
  
  
  METHODS
  Twenty-four rabbits were assigned to the control, high lipid diet (HLD) and OLE group that were fed with standard diet, HLD and HLD supplemented with OLE, respectively. Serum levels of atherosclerosis related markers, triglyceride (TG), total cholesterol (T-CHO), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C) and malondialdehyde (MDA) were detected at the ends of week 2, 4 and 6. Surface lesions and thickness of intimas were measured at the end of week6. The protein and/or mRNA expressions of inflammation factors, monocyte chemoattractant protein (MCP)-1, vascular cell adhesion molecule (VCAM)-1, nuclear factor-kappa B (NF-kappaB) and tumor necrosis factor alpha (TNF-alpha) were investigated by immunohistochemistry and RT-PCR.
  
  
  RESULTS
  Atherosclerotic lesions were found in the HLD and OLE groups but not in the control group. In comparison with that in the HLD group, reduced size and thickness of intima (0.31 +/- 0.26 in the HLD group versus 0.10 +/- 0.03 mm in the OLE group) were found in the OLE group. The MDA level, an indicator of antioxidant status, was 35.27 +/- 15.37 in the HLD group and 20.63 +/- 11.52 nmol/ml in the OLE group. The level of CHO, TG and LDL-C were 104.46 +/- 30.34, 2.48 +/- 1.11, 82.83 +/- 28.44 mmol/l in the HLD group versus 83.03 +/- 27.23, 1.84 +/- 0.44, 59.51 +/- 23.72 mmol/l in the OLE group. Down-regulated expressions of MCP-1, VCAM-1, NF-kappaB and TNF-alpha at both protein and mRNA level (P < 0.05) were also found with the administration of OLE.
  
  
  CONCLUSIONS
  This study proved the effect of OLE on inhibition of atherosclerosis, which is related to the suppressed inflammatory response.
authors.affiliation: Dept of Pathology, Dalian Medical University, Dalian, China.
authors.forename: Lihui
authors.initials: L
authors.lastname: Wang
authors.forename: Chengyan
authors.initials: C
authors.lastname: Geng
authors.forename: Liping
authors.initials: L
authors.lastname: Jiang
authors.forename: Dezheng
authors.initials: D
authors.lastname: Gong
authors.forename: Dayu
authors.initials: D
authors.lastname: Liu
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Yoshimura
authors.forename: Laifu
authors.initials: L
authors.lastname: Zhong
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000097:blood / Q000188:drug therapy* / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D004032:Diet; D006937:Hypercholesterolemia / Q000150:complications / Q000378:metabolism; D007249:Inflammation / Q000097:blood / Q000188:drug therapy* / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D031658:Olea / Q000737:chemistry*; D010936:Plant Extracts / Q000494:pharmacology*; D018515:Plant Leaves / Q000737:chemistry; D011817:Rabbits; D011897:Random Allocation; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D016328:NF-kappa B; D010936:Plant Extracts; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D008315:Malondialdehyde; D002784:Cholesterol