title: Effect of sodium houttuyfonate on myocardial hypertrophy in mice and rats.
abstract: OBJECTIVE
  The aim of the study was to determine the effect of sodium houttuyfonate on myocardial hypertrophy and its mechanism of action in mice and rats.
  
  
  METHODS
  A mouse model of myocardial hypertrophy was established by subcutaneous injection with isoproterenol. Mice were randomly divided into five groups: normal control; isoproterenol control; isoproterenol plus metoprolol; isoproterenol plus low- and high-dose sodium houttuyfonate. A rat model of myocardial hypertrophy was established by intraperitoneal injection with L-thyroxine. Rats were randomly divided into five groups: normal control; L-thyroxine control; L-thyroxine plus captopril; L-thyroxine plus low- and high-dose sodium houttuyfonate. At the end of the experiments, the left ventricular weight index and heart weight index were determined in mice and rats, the size of cardiomyocytes was measured in rats and the concentrations of cAMP in plasma and angiotensin II in ventricular tissue of mice were detected by radioimmunoassay. The endothelin-1 concentration was measured by radioimmunoassay and the hydroxyproline content was measured by a digestive method in ventricular tissue of rats.
  
  
  RESULTS
  After 7-9 days of treatment, sodium houttuyfonate significantly reduced the left ventricular weight index and heart weight index in mice and rats with myocardial hypertrophy, decreased the size of cardiomyocytes in rats, and reduced the content of cAMP and angiotensin II in mice with myocardial hypertrophy. It also decreased the endothelin-1 concentration and the hydroxyproline content in ventricular tissue in rats.
  
  
  CONCLUSIONS
  Sodium houttuyfonate can inhibit myocardial hypertrophy in mouse and rat models by restricting the activity of the sympathetic nervous system and decreasing the levels of angiotensin II and endothelin-1 in ventricular tissue.
authors.affiliation: Department of Pharmacology, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
authors.forename: Jian Ping
authors.initials: JP
authors.lastname: Gao
authors.forename: Chang Xun
authors.initials: CX
authors.lastname: Chen
authors.forename: Ying
authors.initials: Y
authors.lastname: Wang
authors.forename: Jian
authors.initials: J
authors.lastname: Lü
authors.forename: Wei Liang
authors.initials: WL
authors.lastname: Gu
mesh_terms: D000473:Alkanes / Q000494:pharmacology*; D000804:Angiotensin II / Q000378:metabolism / Q000494:pharmacology; D000818:Animals; D002216:Captopril / Q000494:pharmacology; D006332:Cardiomegaly / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control*; D000242:Cyclic AMP / Q000097:blood; D004305:Dose-Response Relationship, Drug; D019332:Endothelin-1 / Q000378:metabolism; D006909:Hydroxyproline / Q000378:metabolism; D007545:Isoproterenol; D008297:Male; D051379:Mice; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000473:pathology; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013447:Sulfites / Q000494:pharmacology*; D013974:Thyroxine
chemical_list: D000473:Alkanes; D019332:Endothelin-1; D013447:Sulfites; C473296:sodium houttuyfonate; D000804:Angiotensin II; D002216:Captopril; D000242:Cyclic AMP; D007545:Isoproterenol; D013974:Thyroxine; D006909:Hydroxyproline