Chapter title |
Taurine Reverses Atrial Structural Remodeling in Ach-Cacl2 Induced Atrial Fibrillation Rats
|
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Chapter number | 65 |
Book title |
Taurine 10
|
Published in |
Advances in experimental medicine and biology, January 2017
|
DOI | 10.1007/978-94-024-1079-2_65 |
Pubmed ID | |
Book ISBNs |
978-9-40-241077-8, 978-9-40-241079-2
|
Authors |
Qunhui Yang, Gaofeng Wu, Limei Han, Ying Feng, Shumei Lin, Qiufeng Lv, Jiancheng Yang, Jianmin Hu, Yang, Qunhui, Wu, Gaofeng, Han, Limei, Feng, Ying, Lin, Shumei, Lv, Qiufeng, Yang, Jiancheng, Hu, Jianmin |
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. |
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