title: Ursolic acid suppresses IL-6 induced C-reactive protein expression in HepG2 and protects HUVECs from injury induced by CRP.
abstract: OBJECTIVE
  To investigate the inhibitory effects of ursolic acid (UA) on the expression of C-reactive protein (CRP) induced by IL-6 in HepG2 cells and the protective effects on the CRP-induced injury to human umbilical vein endothelial cells (HUVECs).
  
  
  METHODS
  HepG2 cells were treated with IL-6 or IL-6 and different concentrations of UA for 48 h, then the cells were collected. The total protein and RNA of the cells were extracted for western blotting and RT-PCR methods to detect CRP protein and mRNA expression. HUVECs were treated with CRP or CRP and different concentrations of UA for 24h. Cell proliferation in each group was assayed by MTT. Cells were collected for western blotting and RT-PCR methods to detect VCAM-1, LOX-1 protein or mRNA expression.
  
  
  RESULTS
  IL-6 can significantly increase CRP protein and mRNA expression in HepG2 cells, and this effect of IL-6 can be decreased by UA (6.25, 12.5, 25 μmol/L) markedly in a dose-dependent manner. UA can inhibit CRP-induced proliferation of HUVECs. CRP can obviously increase LOX-1/VCAM-1 expression in HUVECs, both on mRNA and protein levels and the effect of CRP can be inhibited by UA (5, 10, 20 μmol/L) in a dose-dependent manner.
  
  
  CONCLUSIONS
  UA can reduce the over expression of CRP in HepG2 cells induced by IL-6 and inhibit the increased expression of VCAM-1 and LOX-1 in HUVECs caused by CRP. Our research suggests that UA can reduce CRP levels in plasma and prevent inflammatory cytokines from injuring endothelial cells by inhibiting the hepatic synthesis of CRP. So UA may have positive significance for prevention and treatment of atherosclerosis and other cardiovascular diseases.
authors: Department of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, 9 West Section, Lvshun South Road, Dalian 116044, Liaoning Province, China.
authors: Yuan-yuan
authors: YY
authors: Lv
authors: Yue
authors: Y
authors: Jin
authors: Guo-zhu
authors: GZ
authors: Han
authors: Yan-xia
authors: YX
authors: Liu
authors: Tao
authors: T
authors: Wu
authors: Peng
authors: P
authors: Liu
authors: Qin
authors: Q
authors: Zhou
authors: Ke-Xin
authors: KX
authors: Liu
authors: Hui-Jun
authors: HJ
authors: Sun
mesh_terms: D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D050197:Atherosclerosis / Q000188:drug therapy / Q000517:prevention & control; D002097:C-Reactive Protein / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D015536:Down-Regulation / Q000187:drug effects*; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D056945:Hep G2 Cells; D022781:Hepatocytes / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D061307:Human Umbilical Vein Endothelial Cells / Q000187:drug effects; D006801:Humans; D015850:Interleukin-6 / Q000378:metabolism*; D009994:Osmolar Concentration; D012333:RNA, Messenger / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D051127:Scavenger Receptors, Class E / Q000378:metabolism; D014315:Triterpenes / Q000494:pharmacology*; D015854:Up-Regulation / Q000187:drug effects; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism; D000097245:Ursolic Acid
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D002097:C-Reactive Protein; D015850:Interleukin-6; D012333:RNA, Messenger; D051127:Scavenger Receptors, Class E; D014315:Triterpenes; D019010:Vascular Cell Adhesion Molecule-1; D000097245:Ursolic Acid; C508600:IL6 protein, human; C495137:OLR1 protein, human