title: Benazepril inhibited the NF-κB and TGF-β networking on LV hypertrophy in rats.
abstract: OBJECTIVE
  Benazepril, an angiotensin-converting enzyme (ACE) inhibitor, has been used to treat hypertension, congestive heart failure, and chronic renal failure. However, its biological activity and mechanism of action in inflammation are not fully identified. The present study was designed to determine the in vivo anti-inflammatory effects of benazepril on LV hypertrophy in rats.
  
  
  METHODS
  LV hypertrophy was produced in rats by abdominal aortic coarctation. They were then divided into the following groups: sham operation; LV hypertrophy; LV hypertrophy+benazepril (1mg/kg in a gavage, once a day for 4 weeks). Both morphological assays (hemodynamic and hemorheological measurement; LV hypertrophy assessment), and molecular assays (protein levels of Collagen type I/III, TNF-α and VCAM-1; TGF-β gene expression; NF-κB or Smad activation; intracellular ROS production) were performed.
  
  
  RESULTS
  The following effects were observed in rats treated with benazepril: (1) marked improvements in hemodynamic and hemorheological parameters; (2) significant reductions in LV hypertrophy, dilatation and fibrosis; (3) significantly attenuated protein levels of Collagen type I/III, TGF-β, TNF-α and VCAM-1, NF-κB or Smad activation, as well as intracellular ROS production.
  
  
  CONCLUSIONS
  These results suggest that the anti-inflammatory properties of benazepril may be ascribed to their down-regulation of both NF-κB and TGF-β signaling pathways by acting on the intracellular ROS production in rats with LV hypertrophy, thus supporting the use of benazepril as an anti-inflammatory agent.
authors.affiliation: Department of Pharmacology, Jiangsu Provincial Hospital of Traditional Chinese Medicine (TCM), Nanjing, China.
authors.forename: Shi-Hai
authors.initials: SH
authors.lastname: Yan
authors.forename: Ning-Wei
authors.initials: NW
authors.lastname: Zhao
authors.forename: Xuan-Xuan
authors.initials: XX
authors.lastname: Zhu
authors.forename: Qiong
authors.initials: Q
authors.lastname: Wang
authors.forename: Hai-Dan
authors.initials: HD
authors.lastname: Wang
authors.forename: Rui
authors.initials: R
authors.lastname: Fu
authors.forename: Yuan
authors.initials: Y
authors.lastname: Sun
authors.forename: Qi-Yi
authors.initials: QY
authors.lastname: Li
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001011:Aorta / Q000601:surgery; D001017:Aortic Coarctation / Q000601:surgery; D001552:Benzazepines / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D024042:Collagen Type I / Q000378:metabolism; D024061:Collagen Type III / Q000378:metabolism; D004789:Enzyme Activation; D006439:Hemodynamics / Q000187:drug effects; D006973:Hypertension / Q000188:drug therapy; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy* / Q000276:immunology; D007249:Inflammation / Q000188:drug therapy / Q000276:immunology; D008297:Male; D016328:NF-kappa B / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D051785:Smad Proteins / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000378:metabolism*; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000893:Anti-Inflammatory Agents; D001552:Benzazepines; D024042:Collagen Type I; D024061:Collagen Type III; D016328:NF-kappa B; D017382:Reactive Oxygen Species; D051785:Smad Proteins; D016212:Transforming Growth Factor beta; D019010:Vascular Cell Adhesion Molecule-1; C044946:benazepril
keywords: Benazepril; LV hypertrophy; NF-κB; ROS; TGF-β