title: American ginseng inhibits vascular smooth muscle cell proliferation via suppressing Jak/Stat pathway.
abstract: ETHNOPHARMCOLOGICAL RELEVANCE: Ginseng, a folk medicine which has been used for thousands of years in Asia, has been promoted for the treatment or prevention of health problems including cardiovascular disease. However, the molecular mechanism of ginseng-induced cardiovascular protection is unclear. Thus, we investigated signaling mechanism by which American ginseng inhibits vascular smooth muscle cell (VSMC) proliferation, a key feature of diverse vascular disease.
  
  
  METHODS
  A standardized crude extract of American ginseng was supplied by the National Research Council of Canada, Institute for National Measurement Standards. Rat aortic smooth muscle cells (RASMCs) were exposed to fetal bovine serum (FBS), platelet derived growth factor (PDGF), insulin, or angiotensin II (Ang II) to induce proliferation that was examined by measuring DNA synthesis and cell numbers. Western blot was applied to determine the activations of Jak, Stat, Akt, and ERK.
  
  
  RESULTS
  American ginseng inhibited RASMC proliferation induced by FBS, PDGF, insulin or Ang II. American ginseng slightly increased both basal and FBS-, PDGF- or Ang II-induced activities of Akt and ERK in RASMCs; however, it dramatically inhibited the activation of Jak2 and Stat3.
  
  
  CONCLUSIONS
  These results demonstrate that American ginseng inhibits VSMC proliferation through suppressing the Jak/Stat pathway.
authors.affiliation: Shandong University Qilu Hospital Research Center for Cell Therapy, Key Laboratory of Cardiovascular Remodeling and Function Research, Qilu Hospital of Shandong University, Jinan 250012, China.
authors.forename: Qi
authors.initials: Q
authors.lastname: Wu
authors.forename: Wenjuan
authors.initials: W
authors.lastname: Wang
authors.forename: Siying
authors.initials: S
authors.lastname: Li
authors.forename: Prakash
authors.initials: P
authors.lastname: Nagarkatti
authors.forename: Mitzi
authors.initials: M
authors.lastname: Nagarkatti
authors.forename: Anthony
authors.initials: A
authors.lastname: Windust
authors.forename: Xing Li
authors.initials: XL
authors.lastname: Wang
authors.forename: Dongqi
authors.initials: D
authors.lastname: Tang
authors.forename: Taixing
authors.initials: T
authors.lastname: Cui
mesh_terms: D000818:Animals; D001011:Aorta / Q000166:cytology; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D053614:Janus Kinase 2 / Q000037:antagonists & inhibitors / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000166:cytology; D032389:Myocytes, Smooth Muscle / Q000187:drug effects* / Q000502:physiology; D005894:Panax; D010936:Plant Extracts / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D050796:STAT3 Transcription Factor / Q000037:antagonists & inhibitors / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D010936:Plant Extracts; D050796:STAT3 Transcription Factor; C494088:Stat3 protein, rat; C507927:Jak2 protein, rat; D053614:Janus Kinase 2