title: [Effect of Antrodia cinnamomea on gene expression related to aortal endothelial injury in rats with hyperlipidemia].
abstract: OBJECTIVE
  To investigate the effect of Antrodia cinnamomea on gene expression related to aortal endothelial injury of rats with hyperlipidemia.
  
  
  METHODS
  Fifty SD rats were randomly divided into five groups: the normal control group (NG), the model group (MG), the antrodia cinnamomea groups of low, middle and high doses (AC-LG, AC-MG, AC-HG, 250, 500, 1 000 mg x kg(-1)). The rats were fed with high-fat diets to establish the hyperlipidemia model. After the drug administration for 10 weeks, their serum lipid, SOD, MDA and ox-LDL, LOX-1, P38 MAPK and NF-kappaB mRNA and protein expression were respectively determined, and the aortal endothelial injury was observed under electron microscope.
  
  
  RESULTS
  In the model group, the contents of TC, TG and LDL-C significant increased (P < 0.01), whereas the content of HDL-C significant decreased (P < 0.01). Compared with the model group, both the AC-M group and the AC-H group showed reduction in endothelial injury and significant decrease in the content of TC, TG and LDL-C (P < 0.05 or P < 0.01). The content of HDL-C increased, but with no significant difference. SOD activity in serum remarkably increased (P < 0.05 or P < 0.01), MDA and ox-LDL levels dramatically decreased (P < 0.05 or P < 0.01).
  
  
  CONCLUSIONS
  A. cinnamomea can alleviate endothelial lipid injury by inhibiting the expressions of LOX-1, P38MAPK and NF-kappaB in aorta and better protect aortal endothelial cells from oxidative lipid injury.
authors.forename: Jie
authors.initials: J
authors.lastname: Qi
authors.forename: Yun
authors.initials: Y
authors.lastname: Tao
authors.forename: Jun
authors.initials: J
authors.lastname: Zhang
authors.forename: Jian
authors.initials: J
authors.lastname: Fu
mesh_terms: D000818:Animals; D055491:Antrodia / Q000737:chemistry*; D001011:Aorta / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D050197:Atherosclerosis / Q000097:blood / Q000235:genetics / Q000517:prevention & control; D001688:Biological Products / Q000494:pharmacology*; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D015870:Gene Expression / Q000187:drug effects*; D006949:Hyperlipidemias / Q000097:blood / Q000235:genetics / Q000517:prevention & control*; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008854:Microscopy, Electron; D016328:NF-kappa B / Q000097:blood / Q000235:genetics / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D051127:Scavenger Receptors, Class E / Q000097:blood / Q000235:genetics / Q000378:metabolism; D013482:Superoxide Dismutase / Q000097:blood; D014280:Triglycerides / Q000097:blood; D048051:p38 Mitogen-Activated Protein Kinases / Q000097:blood / Q000235:genetics / Q000378:metabolism
chemical_list: D001688:Biological Products; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D008077:Lipoproteins, LDL; D016328:NF-kappa B; C495136:OLR1 protein, rat; D051127:Scavenger Receptors, Class E; D014280:Triglycerides; C099252:oxidized low density lipoprotein; D008315:Malondialdehyde; D002784:Cholesterol; D013482:Superoxide Dismutase; D048051:p38 Mitogen-Activated Protein Kinases