title: Epigallocatechin-3-gallate inhibits angiotensin II and interleukin-6-induced C-reactive protein production in macrophages.
abstract: BACKGROUND
  Consumption of green tea has been associated with health benefits against multiple diseases including cardiovascular diseases. However, the action mechanisms of green tea and its major ingredient epigallocatechin-3-gallate (EGCG) against cardiovascular diseases are still unclear. Emerging evidence has suggested a common role for C-reactive protein (CRP) in the pathogenesis of inflammation and atherosclerosis. Therefore, the effect of EGCG on angiotensin II (Ang II)- and interleukin-6 (IL-6)-induced CRP production in U937 macrophages and the possible mechanisms were observed.
  
  
  METHODS
  U937 macrophages were cultured, and Ang II and IL-6 were used as stimulants for generation of CRP. U937 macrophages were preincubated with EGCG at 1, 3, 10 μM for 1 h prior to the stimulation. mRNA expression and protein level were determined by RT-PCR and ELISA, respectively. ROS production was observed by a fluorescence microscope.
  
  
  RESULTS
  Pretreatment of macrophages with EGCG prior to the stimulation concentration-dependently inhibited Ang II- and IL-6-induced expression of CRP both in protein and mRNA levels. Meanwhile, EGCG reduced Ang II- and IL-6-stimulated generation of ROS in macrophages.
  
  
  CONCLUSIONS
  EGCG is able to inhibit Ang II- and IL-6-stimulated CRP expression in macrophages to produce an anti-inflammation by interfering with ROS generation. The finding is helpful to update understanding of anti-atherosclerotic effects of EGCG.
authors.affiliation: Department of Pharmacology, Xi'an Jiaotong University School of Medicine, Xi'an, People's Republic of China.
authors.forename: Ming
authors.initials: M
authors.lastname: Li
authors.forename: Jun-Tian
authors.initials: JT
authors.lastname: Liu
authors.forename: Xiao-Ming
authors.initials: XM
authors.lastname: Pang
authors.forename: Chun-Jie
authors.initials: CJ
authors.lastname: Han
authors.forename: Jun-Jun
authors.initials: JJ
authors.lastname: Mao
mesh_terms: D000804:Angiotensin II / Q000235:genetics / Q000378:metabolism*; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D002097:C-Reactive Protein / Q000096:biosynthesis* / Q000235:genetics; D002318:Cardiovascular Diseases / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D045744:Cell Line, Tumor; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism*; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics; D017382:Reactive Oxygen Species / Q000378:metabolism; D013662:Tea; D020298:U937 Cells
chemical_list: D000893:Anti-Inflammatory Agents; D015850:Interleukin-6; D012333:RNA, Messenger; D017382:Reactive Oxygen Species; D013662:Tea; D000804:Angiotensin II; D002392:Catechin; D002097:C-Reactive Protein; C045651:epigallocatechin gallate