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Lemnalol Modulates the Electrophysiological Characteristics and Calcium Homeostasis of Atrial Myocytes

1
Department of Marine Biotechnology and Resources, National Sun Yat-Sen University, Kaohsiung 80424, Taiwan
2
Department of Traditional Medicine, Jianan Mental Hospital, Tainan 717, Taiwan
3
Department of Physiology and Biophysics, National Defense Medical Center, Taipei 114, Taiwan
4
Division of Cardiovascular Surgery, Department of Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan
5
Department of Biomedical Engineering, National Defense Medical Center, Taipei 114, Taiwan
6
Division of Cardiology, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan
*
Author to whom correspondence should be addressed.
Mar. Drugs 2019, 17(11), 619; https://doi.org/10.3390/md17110619
Received: 26 September 2019 / Revised: 26 October 2019 / Accepted: 29 October 2019 / Published: 30 October 2019
Sepsis, an inflammatory response to infection provoked by lipopolysaccharide (LPS), is associated with high mortality, as well as ischemic stroke and new-onset atrial arrhythmia. Severe bacterial infections causing sepsis always result in profound physiological changes, including fever, hypotension, arrhythmia, necrosis of tissue, systemic multi-organ dysfunction and finally death. LPS challenge-induced inflammatory responses during sepsis may increase the likelihood of the arrhythmogenesis. Lemnalol is known to possess potent anti-inflammatory effects. This study examined whether Lemnalol (0.1 μM) could modulate the electrophysiological characteristics and calcium homeostasis of atrial myocytes under the influence of LPS (1μg/mL). Under challenge with LPS, Lemnalol-treated LA myocytes, had a longer AP duration at 20%, 50% and 90% repolarization of the amplitude, compared to the LPS-treated cells. LPS-challenged LA myocytes showed increased late sodium current, Na+-Ca2+ exchanger current, transient outward current, rapid component of delayed rectifier potassium current, tumor necrosis factor-α, NF-κB and increased phosphorylation of ryanodine receptor (RyR), but a lower L-type Ca2+ current than the control LA myocytes. Exposure to Lemnalol reversed the LPS-induced effects. The LPS-treated and control groups of LA myocytes, with or without the existence of Lemnalol. showed no apparent alterations in the sodium current amplitude or Cav1.2 expression. The expression of sarcoendoplasmic reticulum calcium transport ATPase (SERCA2) was reduced by LPS treatment, while Lemnalol ameliorated the LPS-induced alterations. The phosphorylation of RyR was enhanced by LPS treatment, while Lemnalol attenuated the LPS-induced alterations. In conclusion, Lemnalol modulates LPS-induced alterations of LA calcium homeostasis and blocks the NF-κB pathways, which may contribute to the attenuation of LPS-induced arrhythmogenesis. View Full-Text
Keywords: Lemnalol; calcium homeostasis; inflammation; sepsis; left atrium cardiomyocyte; ionic current Lemnalol; calcium homeostasis; inflammation; sepsis; left atrium cardiomyocyte; ionic current
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Tai, B.-Y.; Wen, Z.-H.; Cheng, P.-Y.; Yang, H.-Y.; Duh, C.-Y.; Chen, P.-N.; Hsu, C.-H. Lemnalol Modulates the Electrophysiological Characteristics and Calcium Homeostasis of Atrial Myocytes. Mar. Drugs 2019, 17, 619.

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