title: (1)H NMR-Based Analysis of Serum Metabolites in Monocrotaline-Induced Pulmonary Arterial Hypertensive Rats.
abstract: OBJECTIVE
  To study the changes of the metabolic profile during the pathogenesis in monocrotaline (MCT) induced pulmonary arterial hypertension (PAH).
  
  
  METHODS
  Forty male Sprague-Dawley (SD) rats were randomly divided into 5 groups (n = 8, each). PAH rats were induced by a single dose intraperitoneal injection of 60 mg/kg MCT, while 8 rats given intraperitoneal injection of 1 ml normal saline and scarified in the same day (W0) served as control. Mean pulmonary arterial pressure (mPAP) was measured through catherization. The degree of right ventricular hypertrophy and pulmonary hyperplasia were determined at the end of first to fourth weeks; nuclear magnetic resonance (NMR) spectra of sera were then acquired for the analysis of metabolites. Principal component analysis (PCA) and orthogonal partial least-squares discriminant analysis (OPLS-DA) were used to discriminate different metabolic profiles.
  
  
  RESULTS
  The prominent changes of metabolic profiles were seen during these four weeks. Twenty specific metabolites were identified, which were mainly involved in lipid metabolism, glycolysis, energy metabolism, ketogenesis, and methionine metabolism. Profiles of correlation between these metabolites in each stage changed markedly, especially in the fourth week. Highly activated methionine and betaine metabolism pathways were selected by the pathway enrichment analysis.
  
  
  CONCLUSIONS
  Metabolic dysfunction is involved in the development and progression of PAH.
authors.affiliation: Fujian Hypertension Research Institute, First Affiliated Hospital of Fujian Medical University, Fuzhou 350005, China.
authors.forename: Taijie
authors.initials: T
authors.lastname: Lin
authors.affiliation: MOE Key Laboratory of Spectrochemical Analysis & Instrumentation, Key Laboratory for Chemical Biology of Fujian Province, College of Chemistry and Chemical Engineering, Xiamen University, Xiamen 361005, China.
authors.forename: Jinping
authors.initials: J
authors.lastname: Gu
authors.affiliation: The Physical Education Department, Xiamen University of Technology, Xiamen 361024, China.
authors.forename: Caihua
authors.initials: C
authors.lastname: Huang
authors.affiliation: Fujian Hypertension Research Institute, First Affiliated Hospital of Fujian Medical University, Fuzhou 350005, China.
authors.forename: Suli
authors.initials: S
authors.lastname: Zheng
authors.affiliation: Fujian Hypertension Research Institute, First Affiliated Hospital of Fujian Medical University, Fuzhou 350005, China.
authors.forename: Xu
authors.initials: X
authors.lastname: Lin
authors.affiliation: Fujian Hypertension Research Institute, First Affiliated Hospital of Fujian Medical University, Fuzhou 350005, China.
authors.forename: Liangdi
authors.initials: L
authors.lastname: Xie
authors.affiliation: MOE Key Laboratory of Spectrochemical Analysis & Instrumentation, Key Laboratory for Chemical Biology of Fujian Province, College of Chemistry and Chemical Engineering, Xiamen University, Xiamen 361005, China.
authors.forename: Donghai
authors.initials: D
authors.lastname: Lin
mesh_terms: D000818:Animals; D062186:Arterial Pressure; D004195:Disease Models, Animal; D018450:Disease Progression; D004734:Energy Metabolism; D006019:Glycolysis; D006976:Hypertension, Pulmonary / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology*; D050356:Lipid Metabolism; D008297:Male; D055442:Metabolome; D008715:Methionine / Q000378:metabolism; D016686:Monocrotaline / Q000009:adverse effects*; D066244:Proton Magnetic Resonance Spectroscopy / Q000379:methods*; D011651:Pulmonary Artery / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D016686:Monocrotaline; D008715:Methionine