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Benazepril inhibited the NF-κB and TGF-β networking on LV hypertrophy in rats.

Abstract：

PURPOSE: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.

journal_name

Immunol Lett

journal_title

Immunology letters

authors

Yan SH,Zhao NW,Zhu XX,Wang Q,Wang HD,Fu R,Sun Y,Li QY

doi

10.1016/j.imlet.2013.05.005

subject

Has Abstract

pub_date

2013-05-01 00:00:00

pages

126-34

issue

2

eissn

0165-2478

issn

1879-0542

pii

S0165-2478(13)00065-5

journal_volume

152

pub_type

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