title: The Effects of 17-Methoxyl-7-Hydroxy-Benzene-Furanchalcone on Pressure Overload-Induced Cardiac Remodeling in Rats and the Endothelial Mechanisms Based on PGI2.
abstract: OBJECTIVE
  The primary objective of this study was to study the effects of 17-methoxyl-7-hydroxy-benzene-furanchalcone (MHBFC) on pressure overload-induced cardiac remodeling in rats, as well as the endothelial mechanisms based on PGI2.
  
  
  METHODS
  Six weeks following surgery, rats were divided randomly into the following groups: a sham group, a model group, an MHBFC 12 mg/kg/day group (MHBFC 12), an indomethacin 2 mg/kg/day group (Indo 2), and an Indo 2+ MHBFC 12 group. The MS 4000 organism signal system was used to record the rats' hemodynamic indices. Additionally, the heart weight was determined, and the cardiac remodeling index was calculated. HE and Masson's stains were utilized to perform histological analyses; the immunofluorescence was used to observe the microvessel density of myocardial tissue; the colorimetric method was used to determine the hydroxyproline content of cardiac tissue; the ELISA method was used to measure the plasma PGI2 content; and transmission electron microscopy was used to observe the ultrastructure of the myocardium.
  
  
  RESULTS
  A hyperdynamic circulation state, cardiac remodeling, decreased microvessel density and decreased plasma PGI2 content were each observed in the model group compared with the sham group, in which any changes in the above parameters were effectively reversed by MHBFC. Single-use Indo administration resulted in the progression of these pathophysiological changes; however, MHBFC prevented the worsening of these parameters.
  
  
  CONCLUSIONS
  MHBFC significantly reverses pressure overload-induced cardiac remodeling, and its mechanism may partially contribute to the amelioration of endothelial cell function and the augmentation of PGI2 synthesis and secretion.
authors.affiliation: Pharmaceutical College, Guangxi Medical University, Nanning, Guangxi, China.
authors.forename: Jianchun
authors.initials: J
authors.lastname: Huang
authors.forename: Xiaojun
authors.initials: X
authors.lastname: Tang
authors.forename: Xingmei
authors.initials: X
authors.lastname: Liang
authors.forename: Qingwei
authors.initials: Q
authors.lastname: Wen
authors.forename: Shijun
authors.initials: S
authors.lastname: Zhang
authors.forename: Feifei
authors.initials: F
authors.lastname: Xuan
authors.forename: Jie
authors.initials: J
authors.lastname: Jian
authors.forename: Xing
authors.initials: X
authors.lastname: Lin
authors.forename: Renbin
authors.initials: R
authors.lastname: Huang
mesh_terms: D000818:Animals; D001012:Aorta, Abdominal / Q000187:drug effects* / Q000473:pathology / Q000601:surgery; D002317:Cardiovascular Agents / Q000494:pharmacology*; D047188:Chalcones / Q000494:pharmacology*; D003251:Constriction, Pathologic / Q000097:blood / Q000188:drug therapy* / Q000473:pathology / Q000601:surgery; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D011464:Epoprostenol / Q000819:agonists / Q000097:blood; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006909:Hydroxyproline / Q000378:metabolism; D007213:Indomethacin / Q000494:pharmacology; D008026:Ligation; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D051381:Rats; D017207:Rats, Sprague-Dawley; D020257:Ventricular Remodeling / Q000187:drug effects*
chemical_list: C578356:17-methoxyl-7-hydroxy-benzene-furanchalcone; D002317:Cardiovascular Agents; D047188:Chalcones; D011464:Epoprostenol; D006909:Hydroxyproline; D007213:Indomethacin