title: Hydroxysafflor Yellow A Promotes Angiogenesis via the Angiopoietin 1/ Tie-2 Signaling Pathway.
abstract: The flowers of Carthamus tinctorius L. are widely used in traditional Chinese medicine to treat cerebrovascular and cardiovascular diseases. Hydroxysafflor yellow A (HSYA), the main constituent of C. tinctorius L. flowers, is known for its multiple biological activities. The present study investigated the effects of HSYA on angiogenesis in vitro and in a mouse hindlimb ischemia model.
  
  
  
  Using human umbilical vein endothelial cells (HUVEC) in vitro and a mouse hindlimb ischemia model in vivo, the angiogenic role of HSYA was evaluated.
  
  
  
  HSYA significantly increased the capillary-like tube formation and migration of HUVEC. HSYA not only induced a rise in the expression of angiopoietin 1 and Tie-2 but it also increased phosphorylation of Tie-2, Akt, and extracellular signal-regulated kinase 1/2. Furthermore, an anti-Tie-2 neutralizing antibody significantly inhibited HSYA-induced HUVEC tube formation and migration. In vivo, the recovery of perfusion of ischemic hindlimb tissue after femoral artery interruption was significantly increased in HSYA-treated mice compared to vehicle controls. Consistent with these results, the arteriole and capillary densities in ischemic gastrocnemius muscles were significantly increased in HSYA-treated mice.
  
  
  
  These results indicate the potential utility of HSYA for the treatment of ischemic diseases.
authors.affiliation: Key Laboratory of the Ministry of Education for Medical Electrophysiology and the Institute of Cardiovascular Research, Southwest Medical University, Luzhou, PR China.
authors.forename: Tangting
authors.initials: T
authors.lastname: Chen
authors.forename: Ni
authors.initials: N
authors.lastname: Chen
authors.forename: Ningbo
authors.initials: N
authors.lastname: Pang
authors.forename: Lamei
authors.initials: L
authors.lastname: Xiao
authors.forename: Yongjie
authors.initials: Y
authors.lastname: Li
authors.forename: Rong
authors.initials: R
authors.lastname: Li
authors.forename: Mao
authors.initials: M
authors.lastname: Luo
authors.forename: Xin
authors.initials: X
authors.lastname: Deng
authors.forename: Meiping
authors.initials: M
authors.lastname: Ren
authors.forename: Jianbo
authors.initials: J
authors.lastname: Wu
authors.forename: Liqun
authors.initials: L
authors.lastname: Wang
mesh_terms: D043925:Angiogenesis Inducing Agents / Q000494:pharmacology*; D042683:Angiopoietin-1 / Q000378:metabolism*; D000818:Animals; D001783:Blood Flow Velocity; D002465:Cell Movement / Q000187:drug effects; D002478:Cells, Cultured; D002599:Chalcone / Q000031:analogs & derivatives* / Q000494:pharmacology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D006614:Hindlimb; D061307:Human Umbilical Vein Endothelial Cells / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D007511:Ischemia / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D008810:Mice, Inbred C57BL; D018482:Muscle, Skeletal / Q000098:blood supply*; D018919:Neovascularization, Physiologic / Q000187:drug effects*; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D011809:Quinones / Q000494:pharmacology*; D042787:Receptor, TIE-2 / Q000378:metabolism*; D012039:Regional Blood Flow; D015398:Signal Transduction / Q000187:drug effects*; D013997:Time Factors
chemical_list: C467630:ANGPT1 protein, human; D043925:Angiogenesis Inducing Agents; D042683:Angiopoietin-1; C467628:Angpt1 protein, mouse; D011809:Quinones; C085278:hydroxysafflor yellow A; D002599:Chalcone; D042787:Receptor, TIE-2; C079086:Tek protein, mouse; D051057:Proto-Oncogene Proteins c-akt; D048049:Extracellular Signal-Regulated MAP Kinases