Rhodiola Inhibits Atrial Arrhythmogenesis in a Heart Failure Model

Shuen Hsin Liu, Ya Wen Hsiao, Eric Chong, Rahul Singhal, Man Cai Fong, Yung Nan Tsai, Chiao Po Hsu, Yao Chang Chen, Yi Jen Chen, Chuen Wang Chiou, Shuo Ju Chiang, Shih Lin Chang, Shih Ann Chen

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Introduction: Rhodiola, a popular plant in Tibet, has been proven to decrease arrhythmia. The aim of this study was to elucidate the molecular mechanism and electrophysiological properties of rhodiola in the suppression of atrial fibrillation. Methods: This study consisted of 3 groups as follows: Group 1: normal control rabbits (n = 5); Group 2: rabbits with heart failure (HF) created by coronary ligation and who received 2 weeks of water orally as a placebo (n = 5); and Group 3: rabbits with HF who received 2 weeks of a rhodiola 270 mg/kg/day treatment orally (n = 5). The monophasic action potential, histology, and real-time polymerase chain reaction (RT-PCR) analysis of ionic channels and PI3K/AKT/eNOS were examined. Results: Compared with the HF group, attenuated atrial fibrosis (35.4 ± 17.4% vs. 16.9 ± 8.4%, P = 0.05) and improved left ventricular (LV) ejection fraction (51.6 ± 3.4% vs. 68.0 ± 0.5%, P = 0.001) were observed in the rhodiola group. The rhodiola group had a shorter ERP (85.3 ± 6.8 vs. 94.3 ± 1.2, P = 0.002), APD90 (89.3 ± 1.5 vs. 112.7 ± 0.7, P < 0.001) in the left atrium (LA), and decreased AF inducibility (0.90 ± 0.04 vs. 0.42 ± 0.04, P < 0.001) compared with the HF group. The mRNA expressions of Kv1.4, Kv1.5, Kv4.3, KvLQT1, Cav1.2, and SERCA2a in the HF LA were up-regulated after rhodiola treatment. The rhodiola-treated HF LA demonstrated higher mRNA expression of PI3K-AKT compared with the HF group. Conclusions: Rhodiola reversed LA electrical remodeling, attenuated atrial fibrosis and suppressed AF in rabbits with HF. The beneficial electrophysiological effect of rhodiola may be related to upregulation of Kv1.4, Kv1.5, Kv4.3, KvLQT1, Cav1.2, SERCA2a, and activation of PI3K/AKT signaling.

Original languageEnglish
Pages (from-to)1093-1101
Number of pages9
JournalJournal of Cardiovascular Electrophysiology
Volume27
Issue number9
DOIs
Publication statusPublished - Sep 1 2016

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Rhodiola
Heart Failure
Heart Atria
Phosphatidylinositol 3-Kinases
Atrial Remodeling
Rabbits
Fibrosis
Tibet
Messenger RNA
Ion Channels
Stroke Volume
Atrial Fibrillation
Action Potentials
Ligation
Cardiac Arrhythmias
Real-Time Polymerase Chain Reaction
Histology
Up-Regulation
Placebos

Keywords

  • atrial fibrillation
  • heart failure
  • PI3K/AKT
  • rhodiola

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Liu, S. H., Hsiao, Y. W., Chong, E., Singhal, R., Fong, M. C., Tsai, Y. N., ... Chen, S. A. (2016). Rhodiola Inhibits Atrial Arrhythmogenesis in a Heart Failure Model. Journal of Cardiovascular Electrophysiology, 27(9), 1093-1101. https://doi.org/10.1111/jce.13026

Rhodiola Inhibits Atrial Arrhythmogenesis in a Heart Failure Model. / Liu, Shuen Hsin; Hsiao, Ya Wen; Chong, Eric; Singhal, Rahul; Fong, Man Cai; Tsai, Yung Nan; Hsu, Chiao Po; Chen, Yao Chang; Chen, Yi Jen; Chiou, Chuen Wang; Chiang, Shuo Ju; Chang, Shih Lin; Chen, Shih Ann.

In: Journal of Cardiovascular Electrophysiology, Vol. 27, No. 9, 01.09.2016, p. 1093-1101.

Research output: Contribution to journalArticle

Liu, SH, Hsiao, YW, Chong, E, Singhal, R, Fong, MC, Tsai, YN, Hsu, CP, Chen, YC, Chen, YJ, Chiou, CW, Chiang, SJ, Chang, SL & Chen, SA 2016, 'Rhodiola Inhibits Atrial Arrhythmogenesis in a Heart Failure Model', Journal of Cardiovascular Electrophysiology, vol. 27, no. 9, pp. 1093-1101. https://doi.org/10.1111/jce.13026
Liu, Shuen Hsin ; Hsiao, Ya Wen ; Chong, Eric ; Singhal, Rahul ; Fong, Man Cai ; Tsai, Yung Nan ; Hsu, Chiao Po ; Chen, Yao Chang ; Chen, Yi Jen ; Chiou, Chuen Wang ; Chiang, Shuo Ju ; Chang, Shih Lin ; Chen, Shih Ann. / Rhodiola Inhibits Atrial Arrhythmogenesis in a Heart Failure Model. In: Journal of Cardiovascular Electrophysiology. 2016 ; Vol. 27, No. 9. pp. 1093-1101.
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abstract = "Introduction: Rhodiola, a popular plant in Tibet, has been proven to decrease arrhythmia. The aim of this study was to elucidate the molecular mechanism and electrophysiological properties of rhodiola in the suppression of atrial fibrillation. Methods: This study consisted of 3 groups as follows: Group 1: normal control rabbits (n = 5); Group 2: rabbits with heart failure (HF) created by coronary ligation and who received 2 weeks of water orally as a placebo (n = 5); and Group 3: rabbits with HF who received 2 weeks of a rhodiola 270 mg/kg/day treatment orally (n = 5). The monophasic action potential, histology, and real-time polymerase chain reaction (RT-PCR) analysis of ionic channels and PI3K/AKT/eNOS were examined. Results: Compared with the HF group, attenuated atrial fibrosis (35.4 ± 17.4{\%} vs. 16.9 ± 8.4{\%}, P = 0.05) and improved left ventricular (LV) ejection fraction (51.6 ± 3.4{\%} vs. 68.0 ± 0.5{\%}, P = 0.001) were observed in the rhodiola group. The rhodiola group had a shorter ERP (85.3 ± 6.8 vs. 94.3 ± 1.2, P = 0.002), APD90 (89.3 ± 1.5 vs. 112.7 ± 0.7, P < 0.001) in the left atrium (LA), and decreased AF inducibility (0.90 ± 0.04 vs. 0.42 ± 0.04, P < 0.001) compared with the HF group. The mRNA expressions of Kv1.4, Kv1.5, Kv4.3, KvLQT1, Cav1.2, and SERCA2a in the HF LA were up-regulated after rhodiola treatment. The rhodiola-treated HF LA demonstrated higher mRNA expression of PI3K-AKT compared with the HF group. Conclusions: Rhodiola reversed LA electrical remodeling, attenuated atrial fibrosis and suppressed AF in rabbits with HF. The beneficial electrophysiological effect of rhodiola may be related to upregulation of Kv1.4, Kv1.5, Kv4.3, KvLQT1, Cav1.2, SERCA2a, and activation of PI3K/AKT signaling.",
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AU - Liu, Shuen Hsin

AU - Hsiao, Ya Wen

AU - Chong, Eric

AU - Singhal, Rahul

AU - Fong, Man Cai

AU - Tsai, Yung Nan

AU - Hsu, Chiao Po

AU - Chen, Yao Chang

AU - Chen, Yi Jen

AU - Chiou, Chuen Wang

AU - Chiang, Shuo Ju

AU - Chang, Shih Lin

AU - Chen, Shih Ann

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N2 - Introduction: Rhodiola, a popular plant in Tibet, has been proven to decrease arrhythmia. The aim of this study was to elucidate the molecular mechanism and electrophysiological properties of rhodiola in the suppression of atrial fibrillation. Methods: This study consisted of 3 groups as follows: Group 1: normal control rabbits (n = 5); Group 2: rabbits with heart failure (HF) created by coronary ligation and who received 2 weeks of water orally as a placebo (n = 5); and Group 3: rabbits with HF who received 2 weeks of a rhodiola 270 mg/kg/day treatment orally (n = 5). The monophasic action potential, histology, and real-time polymerase chain reaction (RT-PCR) analysis of ionic channels and PI3K/AKT/eNOS were examined. Results: Compared with the HF group, attenuated atrial fibrosis (35.4 ± 17.4% vs. 16.9 ± 8.4%, P = 0.05) and improved left ventricular (LV) ejection fraction (51.6 ± 3.4% vs. 68.0 ± 0.5%, P = 0.001) were observed in the rhodiola group. The rhodiola group had a shorter ERP (85.3 ± 6.8 vs. 94.3 ± 1.2, P = 0.002), APD90 (89.3 ± 1.5 vs. 112.7 ± 0.7, P < 0.001) in the left atrium (LA), and decreased AF inducibility (0.90 ± 0.04 vs. 0.42 ± 0.04, P < 0.001) compared with the HF group. The mRNA expressions of Kv1.4, Kv1.5, Kv4.3, KvLQT1, Cav1.2, and SERCA2a in the HF LA were up-regulated after rhodiola treatment. The rhodiola-treated HF LA demonstrated higher mRNA expression of PI3K-AKT compared with the HF group. Conclusions: Rhodiola reversed LA electrical remodeling, attenuated atrial fibrosis and suppressed AF in rabbits with HF. The beneficial electrophysiological effect of rhodiola may be related to upregulation of Kv1.4, Kv1.5, Kv4.3, KvLQT1, Cav1.2, SERCA2a, and activation of PI3K/AKT signaling.

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KW - atrial fibrillation

KW - heart failure

KW - PI3K/AKT

KW - rhodiola

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