title: Picrorhiza scrophulariiflora improves accelerated atherosclerosis through inhibition of redox-sensitive inflammation.
abstract: BACKGROUND
  Accumulation of advanced glycation end products (AGEs) or advanced oxidation protein products (AOPPs) has been identified as a risk factor for accelerated atherosclerosis seen in diabetes and chronic kidney disease. However, little is known about the intervention for atherogenesis associated with these oxidized proteins. The rhizome of Picrorhiza scrophulariiflora (PS) has long been used to treat inflammatory diseases as a traditional medication. The study was performed to test the hypothesis that ethanol extraction of PS (EPS) may improve AGEs- or AOPPs-induced accelerated atherosclerosis in vivo.
  
  
  RESULTS
  Hypercholesterolemic or normal rabbits were randomly assigned to 8 groups treated with intravenous injection of AGEs- or AOPPs-modified rabbit serum albumin (AGEs-RSA or AOPPs-RSA), unmodified RSA or vehicle in the presence or absence of EPS (10 mg/kg/2 days) gavage for 10 weeks. Compared with hypercholesterolemic rabbits without EPS treatment, EPS administration significantly decreased the aortic plaque volume and oxidized low density lipoprotein (Ox-LDL) deposition in hypercholesterolemic animals. This was accompanied by significant histological improvement including decrease of intimal and smooth muscle cell proliferation and macrophage influx in affected areas. EPS administration almost completely abolished the accelerated atherosclerosis induced by chronic treatment of AGEs- or AOPPs-RSA in both hypercholesterolemic and normal rabbits. EPS administration significantly restored the AGEs- or AOPPs-induced redox imbalance and inflammation, evidenced by decrease of plasma Ox-LDL, thiobarbituric acid reactive substances and TNF-alpha, and increase of glutathione peroxidase activity.
  
  
  CONCLUSIONS
  These data suggested that EPS may improve atherosclerosis, particularly that induced by AGEs or AOPPs, through inhibition of redox-sensitive inflammation.
authors.affiliation: Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, PR China.
authors.forename: Zhi Jian
authors.initials: ZJ
authors.lastname: Guo
authors.forename: Fan Fan
authors.initials: FF
authors.lastname: Hou
authors.forename: Shang Xi
authors.initials: SX
authors.lastname: Liu
authors.forename: Jian Wei
authors.initials: JW
authors.lastname: Tian
authors.forename: Wei Ru
authors.initials: WR
authors.lastname: Zhang
authors.forename: Di
authors.initials: D
authors.lastname: Xie
authors.forename: Zhan Mei
authors.initials: ZM
authors.lastname: Zhou
authors.forename: Zhi Qiang
authors.initials: ZQ
authors.lastname: Liu
authors.forename: Xun
authors.initials: X
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001018:Aortic Diseases / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism; D050197:Atherosclerosis / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism*; D004195:Disease Models, Animal; D004365:Drugs, Chinese Herbal / Q000494:pharmacology*; D005260:Female; D005979:Glutathione Peroxidase / Q000378:metabolism; D017127:Glycation End Products, Advanced / Q000097:blood; D006937:Hypercholesterolemia / Q000276:immunology / Q000378:metabolism; D008077:Lipoproteins, LDL / Q000097:blood; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects*; D032261:Picrorhiza; D011817:Rabbits; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D004365:Drugs, Chinese Herbal; D017127:Glycation End Products, Advanced; D008077:Lipoproteins, LDL; D017392:Thiobarbituric Acid Reactive Substances; D014409:Tumor Necrosis Factor-alpha; C099252:oxidized low density lipoprotein; D005979:Glutathione Peroxidase