title: Hydroxysafflor yellow A improves established monocrotaline-induced pulmonary arterial hypertension in rats.
abstract: OBJECTIVE
  To evaluate the beneficial effects of hydroxysafflor yellow A (HSYA) on monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH) in rats, and to investigate the main pathophysiological mechanism of HSYA in preventing development of MCT-induced PAH.
  
  
  METHODS
  Four groups (control, control with HSYA treatment, MCT-exposed, and MCT-exposed with HSYA treatment) were evaluated at day 28 following MCT exposure. Haemodynamic measurements, right ventricular hypertrophy, morphometry, inflammatory cytokines and oxidant expression were assessed.
  
  
  RESULTS
  HSYA significantly reduced haemodynamic changes, right ventricular hypertrophy and morphometric changes induced by exposure to MCT. HYSA also suppressed MCT-induced inflammation and oxidative stress in rat pulmonary tissue.
  
  
  CONCLUSIONS
  Experimental MCT-induced PAH may be reduced by HSYA treatment, and the mechanism may involve suppression of inflammation and oxidative stress.
authors.affiliation: Hunan Provincial People's Hospital, Changsha, Hunan province, China.
authors.forename: Xiaotong
authors.initials: X
authors.lastname: Han
authors.affiliation: Hunan Provincial People's Hospital, Changsha, Hunan province, China zhangyixiong198@126.com.
authors.forename: Yixiong
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Hunan Provincial People's Hospital, Changsha, Hunan province, China.
authors.forename: Zhou
authors.initials: Z
authors.lastname: Zhou
authors.affiliation: Hunan Provincial People's Hospital, Changsha, Hunan province, China.
authors.forename: Xingwen
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Hunan Provincial People's Hospital, Changsha, Hunan province, China.
authors.forename: Yanfei
authors.initials: Y
authors.lastname: Long
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000818:Animals; D002599:Chalcone / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D006976:Hypertension, Pulmonary / Q000150:complications / Q000188:drug therapy* / Q000235:genetics / Q000503:physiopathology; D017380:Hypertrophy, Right Ventricular / Q000150:complications / Q000188:drug therapy / Q000235:genetics / Q000503:physiopathology; D007249:Inflammation / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D016686:Monocrotaline; D018384:Oxidative Stress / Q000187:drug effects; D011809:Quinones / Q000494:pharmacology / Q000627:therapeutic use*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D066253:Vascular Remodeling / Q000187:drug effects
chemical_list: D011809:Quinones; D012333:RNA, Messenger; C085278:hydroxysafflor yellow A; D008315:Malondialdehyde; D002599:Chalcone; D016686:Monocrotaline; D000080242:8-Hydroxy-2'-Deoxyguanosine; D013482:Superoxide Dismutase; D003849:Deoxyguanosine
keywords: Chinese medicine; hydroxysafflor; inflammation; monocrotaline; oxidant; pulmonary artery hypertension; safflower