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Inhibition of inflammation contributes to organ protection of atenolol in sinoaortic-denervated rats.

Authors
  • Zhang, Chuan
  • Xie, He-Hui
  • Lu, Ze-An
  • Zhu, Min-Juan
  • Su, Ding-Feng
Type
Published Article
Journal
Journal of Cardiovascular Pharmacology
Publisher
Ovid Technologies (Wolters Kluwer) - Lippincott Williams & Wilkins
Publication Date
May 01, 2004
Volume
43
Issue
5
Pages
663–668
Identifiers
PMID: 15071353
Source
Medline
License
Unknown

Abstract

The present study was designed to test the hypothesis that inhibition of inflammation contributes to the protective effects of atenolol on the organ damage induced by sinoaortic denervation (SAD) in rats. SAD was performed in male Sprague-Dawley rats at the age of 10 weeks. Atenolol (20 mg/kg/d, po) was administered for 12 weeks beginning from 4 weeks after SAD. Organ damage evaluation and the determination of plasma TXB2, serum IL-1, TNF-alpha and tissue reactive oxygen species (ROS) were performed at 16 weeks after SAD. It was found that there existed obvious organ damage including increased cardiac and aortic collagen, and glomerular injury, in SAD rats. Plasma TXB2, serum TNF-alpha IL-1, and tissue ROS increased significantly after SAD. Long-term treatment with atenolol significantly prevented the organ damage with a decrease in left ventricular weight, cardiac and aortic collagen contents, and glomerular injury score in SAD rats. Plasma TXB2, serum IL-1, and tissue ROS were found to be significantly decreased by the long-term treatment with atenolol. Furthermore, it was found that the levels of inflammation-related factors were significantly related to all the organ-damage parameters studied in this experiment. These results suggest that inhibition of inflammation and oxygen stress contributes to the organ-protective effects of atenolol in SAD rats.

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