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Taurine 10 pp 831-841 | Cite as

Taurine Reverses Atrial Structural Remodeling in Ach-Cacl2 Induced Atrial Fibrillation Rats

  • Qunhui Yang
  • Gaofeng Wu
  • Limei Han
  • Ying Feng
  • Shumei Lin
  • Qiufeng Lv
  • Jiancheng Yang
  • Jianmin HuEmail author
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 975)

Abstract

Taurine has been reported to have anti-arrhythmia effects, but the anti-atrial fibrillation (AF) effects and its mechanism remain incompletely understood. In the present study, the therapy effects and partly mechanisms were investigated. AF animal model was established by intravenous administered with the mixture of acetylcholine (Ach) and CaCl2 (66 μg/mL + 10 mg/mL) (i.v.) for 7 days. The actions of taurine (99 mg/kg∙d, introgastric administration) on the levels of Hs-CRP, IL-6, TNF-α, MMP-9, AngII, the extent of the fibrosis and ultrastructural changes in left atrial were studied. The data showed that the serum levels of TNF-α, IL-6, AngII and the plasma levels of Hs-CRP and MMP-9 were significantly elevated in automatic recovery group relative to the control group (p < 0.01), which were all decreased by taurine administration (p < 0.01) similar to Verapamil treatment. Masson’s trichrome staining of the left atrial tissue showed an obvious interstitial fibrosis in rats of automatic recovery group. The alteration could be reversed by additional taurine. Electron microscopy revealed that taurine administration could significantly alleviate the ultrastructural damage of atrial cells, and the effects were similar to the Verapamil treatment. In conclusion, the results suggested that taurine could inhibit the structural remodeling of AF in rats partly by decreasing the levels of inflammatory factors and profibrotic molecules, attenuating the extent of myocardial fibrosis and protecting the integrity of myocardial ultrastructure.

Keywords

Taurine Atrial fibrillation Inflammatory factors Fibrosis Ultrastructure 

Abbreviations

Ach

Acetylcholine

AF

Atrial fibrillation

AngII

Angiotensin II

Hs-CRP

High-sensitive C-reactive protein

IL-6

Interleukin-6

MMP-9

Matrix metallaproteinase-9

MMPs

Matrix metalloproteinases

TNF-α

Tumor necrosis factor-α

Notes

Acknowledgments

This research was supported by grants from the National Natural Science Foundation (No. 31502026, No. 31302051, No. 31402160) of China and Cultivation Plan for Youth Agricultural Science and Technology Innovative Talents of Liaoning Province (No. 2014049).

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Copyright information

© Springer Science+Business Media B.V. 2017

Authors and Affiliations

  • Qunhui Yang
    • 1
  • Gaofeng Wu
    • 1
  • Limei Han
    • 1
  • Ying Feng
    • 1
  • Shumei Lin
    • 1
  • Qiufeng Lv
    • 1
  • Jiancheng Yang
    • 1
  • Jianmin Hu
    • 1
    Email author
  1. 1.Liaoning Provincial Key Laboratory of Zoonosis, College of Animal Science and Veterinary MedicineShenyang Agricultural UniversityShenyangPeople’s Republic of China

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