Taurine Reverses Atrial Structural Remodeling in Ach-Cacl2 Induced Atrial Fibrillation Rats
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.
KeywordsTaurine Atrial fibrillation Inflammatory factors Fibrosis Ultrastructure
High-sensitive C-reactive protein
Tumor necrosis factor-α
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).
- Balasubramanian S, Fan M, Messmer-Blust AF, Yang CH, Trendel JA, Jeyaratnam JA, Pfeffer LM, Vestal DJ (2011) The interferon-γ-induced GTPase, mGBP-2, inhibits TNF-α induction of matrix metalloproteinase-9 (MMP-9) by inhibiting NF-κB and Rac. J Biol Chem 286:20054–20064CrossRefPubMedPubMedCentralGoogle Scholar
- Chen CL, Gong TT, Tang YQ, Kou YY, Yu P, Shao R, Zhang CF (2009) Establishment of atrial fibrillation model in SD rats. Lab Anim Sci 26(3):1–4Google Scholar
- Go AS, Hylek EM, Phillips KA, Chang Y, Henault LE, Selby JV, Singer DE (2001) Prevalence of diagnosed atrial fibrillation in adults: national implications for rhythm management and stroke prevention: the AnTicoagulation and Risk Factors in Atrial Fibrillation (ATRIA) Study. JAMA 285:2370–2375CrossRefPubMedGoogle Scholar
- Ito T, Kimura Y, Uozumi Y, Takai M, Muraoka S, Matsuda T, Ueki K, Yoshiyama M, Ikawa M, Okabe M, Schaffer SW, Fujio Y, Azuma J (2008) Taurine depletion caused by knocking out the taurine transporter gene leads to cardiomyopathy with cardiac atrophy. J Mol Cell Cardiol 44:927–937Google Scholar
- Learn DB, Fried VA, Thomas EL (1996) Taurine and hypotaurine contents of human leukocytes. J Leukoc Biol 48:174–182Google Scholar
- Saba S, Janczewski AM, Baker LC, Shusterman V, Gursoy EC, Feldman AM, Salama G, McTiernan CF, London B (2005) Atrial contractile dysfunction, fibrosis, and arrhythmias in a mouse model of cardiomyopathy secondary to cardiac-specific overexpression of tumor necrosis factor-α. Am J Physiol Heart Circ Physiol 289(4):H1456–H1467CrossRefPubMedGoogle Scholar