title: The antioxidant N-2-mercaptopropionyl glycine attenuates left ventricular hypertrophy in in vivo murine pressure-overload model.
abstract: OBJECTIVE
  In order to identify the role of reactive oxygen species (ROS) in cardiac hypertrophy, we examined the effect of N-2-mercaptopropionyl glycine (MPG) on cardiac hypertrophy.
  
  
  BACKGROUND
  Recent in vitro studies have suggested that ROS play an important role as a second messenger in cardiac hypertrophy. It was therefore thought to be of particular value to examine the relevance of studies using in vitro models for cardiac hypertrophy in an in vivo setting.
  
  
  METHODS
  The transverse thoracic aorta in mice was constricted, and MPG (100 mg/kg) was infused intraperitoneally twice daily. The animals were assessed seven days after the operation for hemodynamic functions, oxidative stress and antioxidative enzyme activities.
  
  
  RESULTS
  Banding of the transverse aorta in mice resulted in an increase in the ratio of heart weight to tibia length and the appearance of an endogenous atrial natriuretic factor messenger ribonucleic acid (mRNA) seven days postoperatively. Administration of MPG significantly attenuated the hypertrophic responses induced by pressure overload. Cardiac hypertrophy was accompanied by increases in heme oxygenase-1 mRNA expression and lipid peroxidation, which was eliminated by the treatment with MPG. Pressure overload led to increases in antioxidant enzyme activities, such as superoxide dismutase and glutathione peroxidase, but not catalase, activity.
  
  
  CONCLUSIONS
  Our results indicated that oxidative stress was increased in our model and that it plays an important role in the development of cardiac hypertrophy.
authors.affiliation: Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Osaka, Japan.
authors.forename: Moto-o
authors.initials: MO
authors.lastname: Date
authors.forename: Takashi
authors.initials: T
authors.lastname: Morita
authors.forename: Nobushige
authors.initials: N
authors.lastname: Yamashita
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Nishida
authors.forename: Osamu
authors.initials: O
authors.lastname: Yamaguchi
authors.forename: Yoshiharu
authors.initials: Y
authors.lastname: Higuchi
authors.forename: Shinichi
authors.initials: S
authors.lastname: Hirotani
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Matsumura
authors.forename: Masatsugu
authors.initials: M
authors.lastname: Hori
authors.forename: Michihiko
authors.initials: M
authors.lastname: Tada
authors.forename: Kinya
authors.initials: K
authors.lastname: Otsu
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000009:adverse effects*; D001013:Aorta, Thoracic / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D003251:Constriction, Pathologic / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D017379:Hypertrophy, Left Ventricular / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D011897:Random Allocation; D017382:Reactive Oxygen Species / Q000009:adverse effects*; D008625:Tiopronin / Q000009:adverse effects*
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species; D008625:Tiopronin