title: Epigallocatechin-3-gallate inhibits interleukin-6- and angiotensin II-induced production of C-reactive protein in vascular smooth muscle cells.
abstract: OBJECTIVE
  Extensive research suggests that atherosclerosis is an inflammatory disease and that epigallocatechin-3-gallate (EGCG) is able to inhibit the formation and development of atherosclerosis. However, the mechanisms of action of EGCG against atherosclerosis are still unclear. Therefore, the effect of EGCG on interleukin-6 (IL-6)- and angiotensin II (Ang II)-induced CRP production in vascular smooth muscle cells (VSMCs) was studied to provide experimental evidence for its anti-inflammatory and anti-atherosclerotic actions.
  
  
  METHODS
  Rat VSMCs were cultured, and IL-6 (10(-7)M) and Ang II (10(-7)M) were used as stimulants for CRP generation. The CRP concentration in the supernatant was measured with ELISA, and mRNA and protein expression of CRP was assayed with RT-qPCR and immunocytochemistry, respectively. The production of reactive oxygen species (ROS) and superoxide anion (O(2)(-)) was detected with ROS and O(2)(-) assay kits, respectively.
  
  
  RESULTS
  The results showed that both IL-6 and Ang II increased CRP levels in the supernatant of VSMCs and induced mRNA and protein expression of CRP in VSMCs, whereas pretreatment of the cells with EGCG (1 x 10(-6)M, 3 x 10(-6)M, 10 x 10(-6)M) significantly inhibited IL-6- and Ang II-induced production and expression of CRP in VSMCs in a concentration-dependent manner. Additionally, Ang II stimulated O(2)(-) and ROS generations in VSMCs, and EGCG decreased the Ang II-induced increase of O(2)(-) and ROS in a concentration-dependent fashion.
  
  
  CONCLUSIONS
  These results suggest that EGCG plays an anti-inflammatory role via inhibiting IL-6- and Ang II-induced CRP secretion, as well as the Ang II-induced generation of O(2)(-) and ROS in VSMCs, which contributes to its anti-atherosclerotic action.
authors.affiliation: Department of Pharmacology, Xi'an Jiaotong University School of Medicine, Xi'an, China.
authors.forename: Ning
authors.initials: N
authors.lastname: Peng
authors.forename: Jun-tian
authors.initials: JT
authors.lastname: Liu
authors.forename: Fang
authors.initials: F
authors.lastname: Guo
authors.forename: Rui
authors.initials: R
authors.lastname: Li
mesh_terms: D000804:Angiotensin II / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001013:Aorta, Thoracic / Q000166:cytology / Q000187:drug effects; D002097:C-Reactive Protein / Q000096:biosynthesis*; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D004797:Enzyme-Linked Immunosorbent Assay; D007150:Immunohistochemistry; D015850:Interleukin-6 / Q000494:pharmacology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism*; D032389:Myocytes, Smooth Muscle / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000093242:Interleukin-6 Inhibitors
chemical_list: D000804:Angiotensin II; D000975:Antioxidants; D002097:C-Reactive Protein; D002392:Catechin; D015850:Interleukin-6; D000093242:Interleukin-6 Inhibitors; C045651:epigallocatechin gallate