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Electroacupuncture at PC6 (Neiguan) Improves Extracellular Signal-Regulated Kinase Signaling Pathways Through the Regulation of Neuroendocrine Cytokines in Myocardial Hypertrophic Rats

Electroacupuncture (EA) therapy has been widely accepted as a useful therapeutic technique with low or no risk in the clinical prevention of cardiac hypertrophy. However, the signaling transduction mechanism underlying this effect remains unclear. The current study investigates the effects of EA on...

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Autores principales: Li, Jia, Li, Jing, Liang, Fengxia, Hong, Yaqun, Wu, Song, Tang, Hongtu, Wang, Hua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3163147/
https://www.ncbi.nlm.nih.gov/pubmed/21876715
http://dx.doi.org/10.1155/2012/792820
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author Li, Jia
Li, Jing
Liang, Fengxia
Hong, Yaqun
Wu, Song
Tang, Hongtu
Wang, Hua
author_facet Li, Jia
Li, Jing
Liang, Fengxia
Hong, Yaqun
Wu, Song
Tang, Hongtu
Wang, Hua
author_sort Li, Jia
collection PubMed
description Electroacupuncture (EA) therapy has been widely accepted as a useful therapeutic technique with low or no risk in the clinical prevention of cardiac hypertrophy. However, the signaling transduction mechanism underlying this effect remains unclear. The current study investigates the effects of EA on the signaling pathways of myocardial hypertrophy (MH) in rats. Up to 40 3-month-old Sprague-Dawley (SD) rats were randomly divided into normal, model, PC6 (Neiguan), and LI4 (Hegu) groups, with ten rats in each group. All the rats except for the normal group received 3 mg/kg·d of isoprinosine hydrochloride (ISO) injection into the back skin. The rats in the PC6 and LI4 groups received EA for 14 days. On the 15th day, electrocardiograms were recorded, and the ultrastructure of the myocardial cells was observed. The myocardial hypertrophy indices (MHIs), electrocardiograph (ECG), ultrastructure observation, levels of plasma angiotensin II (Ang II) and endothelin (ET), as well as protein expression of extracellular signal-regulated kinase (ERK), and phosphorylation extracellular signal regulating kinase (p-ERK) in the left ventricular myocardial tissue were measured. The results indicated that EA can improve cardiac function in MH rats by modulating upstream neuroendocrine cytokines that regulate the ERK signaling pathways.
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spelling pubmed-31631472011-08-29 Electroacupuncture at PC6 (Neiguan) Improves Extracellular Signal-Regulated Kinase Signaling Pathways Through the Regulation of Neuroendocrine Cytokines in Myocardial Hypertrophic Rats Li, Jia Li, Jing Liang, Fengxia Hong, Yaqun Wu, Song Tang, Hongtu Wang, Hua Evid Based Complement Alternat Med Research Article Electroacupuncture (EA) therapy has been widely accepted as a useful therapeutic technique with low or no risk in the clinical prevention of cardiac hypertrophy. However, the signaling transduction mechanism underlying this effect remains unclear. The current study investigates the effects of EA on the signaling pathways of myocardial hypertrophy (MH) in rats. Up to 40 3-month-old Sprague-Dawley (SD) rats were randomly divided into normal, model, PC6 (Neiguan), and LI4 (Hegu) groups, with ten rats in each group. All the rats except for the normal group received 3 mg/kg·d of isoprinosine hydrochloride (ISO) injection into the back skin. The rats in the PC6 and LI4 groups received EA for 14 days. On the 15th day, electrocardiograms were recorded, and the ultrastructure of the myocardial cells was observed. The myocardial hypertrophy indices (MHIs), electrocardiograph (ECG), ultrastructure observation, levels of plasma angiotensin II (Ang II) and endothelin (ET), as well as protein expression of extracellular signal-regulated kinase (ERK), and phosphorylation extracellular signal regulating kinase (p-ERK) in the left ventricular myocardial tissue were measured. The results indicated that EA can improve cardiac function in MH rats by modulating upstream neuroendocrine cytokines that regulate the ERK signaling pathways. Hindawi Publishing Corporation 2012 2011-08-24 /pmc/articles/PMC3163147/ /pubmed/21876715 http://dx.doi.org/10.1155/2012/792820 Text en Copyright © 2012 Jia Li et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Li, Jia
Li, Jing
Liang, Fengxia
Hong, Yaqun
Wu, Song
Tang, Hongtu
Wang, Hua
Electroacupuncture at PC6 (Neiguan) Improves Extracellular Signal-Regulated Kinase Signaling Pathways Through the Regulation of Neuroendocrine Cytokines in Myocardial Hypertrophic Rats
title Electroacupuncture at PC6 (Neiguan) Improves Extracellular Signal-Regulated Kinase Signaling Pathways Through the Regulation of Neuroendocrine Cytokines in Myocardial Hypertrophic Rats
title_full Electroacupuncture at PC6 (Neiguan) Improves Extracellular Signal-Regulated Kinase Signaling Pathways Through the Regulation of Neuroendocrine Cytokines in Myocardial Hypertrophic Rats
title_fullStr Electroacupuncture at PC6 (Neiguan) Improves Extracellular Signal-Regulated Kinase Signaling Pathways Through the Regulation of Neuroendocrine Cytokines in Myocardial Hypertrophic Rats
title_full_unstemmed Electroacupuncture at PC6 (Neiguan) Improves Extracellular Signal-Regulated Kinase Signaling Pathways Through the Regulation of Neuroendocrine Cytokines in Myocardial Hypertrophic Rats
title_short Electroacupuncture at PC6 (Neiguan) Improves Extracellular Signal-Regulated Kinase Signaling Pathways Through the Regulation of Neuroendocrine Cytokines in Myocardial Hypertrophic Rats
title_sort electroacupuncture at pc6 (neiguan) improves extracellular signal-regulated kinase signaling pathways through the regulation of neuroendocrine cytokines in myocardial hypertrophic rats
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3163147/
https://www.ncbi.nlm.nih.gov/pubmed/21876715
http://dx.doi.org/10.1155/2012/792820
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