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Attenuated Cardiac Mitochondrial-Dependent Apoptotic Effects by Li-Fu Formula in Hamsters Fed with a Hypercholesterol Diet

Apoptosis involves in the pathogenesis of various cardiac abnormalities. This study intends to evaluate the effects of Li-Fu formula on cardiac apoptosis induced by hyper-cholesterol diet. Twenty-four male Golden Syrian hamsters were randomly divided into Control, Cholesterol and Li-Fu formula group...

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Autores principales: Kuo, Wei-Wen, Hsu, Tsai-Ching, Chain, Mei-Haung, Lai, Chao-Hung, Wang, Wen-Hong, Tsai, Fuu-Jen, Tsai, Chang-Hai, Wu, Chieh-His, Huang, Chih-Yang, Tzang, Bor-Show
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3135794/
https://www.ncbi.nlm.nih.gov/pubmed/19939950
http://dx.doi.org/10.1093/ecam/nep182
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author Kuo, Wei-Wen
Hsu, Tsai-Ching
Chain, Mei-Haung
Lai, Chao-Hung
Wang, Wen-Hong
Tsai, Fuu-Jen
Tsai, Chang-Hai
Wu, Chieh-His
Huang, Chih-Yang
Tzang, Bor-Show
author_facet Kuo, Wei-Wen
Hsu, Tsai-Ching
Chain, Mei-Haung
Lai, Chao-Hung
Wang, Wen-Hong
Tsai, Fuu-Jen
Tsai, Chang-Hai
Wu, Chieh-His
Huang, Chih-Yang
Tzang, Bor-Show
author_sort Kuo, Wei-Wen
collection PubMed
description Apoptosis involves in the pathogenesis of various cardiac abnormalities. This study intends to evaluate the effects of Li-Fu formula on cardiac apoptosis induced by hyper-cholesterol diet. Twenty-four male Golden Syrian hamsters were randomly divided into Control, Cholesterol and Li-Fu formula groups. Histopathological analysis, western blotting and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays were performed to measure the effects of Li-Fu formula on left ventricle. Significantly reduced TUNEL-positive cells and mitochondria- dependent apoptosis were observed in the left ventricle of hamsters from Li-Fu formula group compared to the Cholesterol group. Additionally, induced cardiac insulin like growth factor I receptor (IGFIR)-dependent survival pathway was detected in the Li-Fu formula group compared to the Cholesterol group. Besides, minor fibrosis, increased collagen deposition, and myofibril disarray was detected in the Cholesterol group, whereas the reductions of collagen deposition and myofibril disarray were observed in the Li-Fu formula group. This study demonstrated that Li-Fu formula not only reduced the mitochondria-dependent apoptosis and fibrosis, but also enhanced the IGF-I survival pathway in the left ventricle from high cholesterol-fed hamsters. We suggest the protective effects of Li-Fu formula on cardiac apoptosis and therapeutic potentials against cardiovascular disease.
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spelling pubmed-31357942011-08-02 Attenuated Cardiac Mitochondrial-Dependent Apoptotic Effects by Li-Fu Formula in Hamsters Fed with a Hypercholesterol Diet Kuo, Wei-Wen Hsu, Tsai-Ching Chain, Mei-Haung Lai, Chao-Hung Wang, Wen-Hong Tsai, Fuu-Jen Tsai, Chang-Hai Wu, Chieh-His Huang, Chih-Yang Tzang, Bor-Show Evid Based Complement Alternat Med Original Article Apoptosis involves in the pathogenesis of various cardiac abnormalities. This study intends to evaluate the effects of Li-Fu formula on cardiac apoptosis induced by hyper-cholesterol diet. Twenty-four male Golden Syrian hamsters were randomly divided into Control, Cholesterol and Li-Fu formula groups. Histopathological analysis, western blotting and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays were performed to measure the effects of Li-Fu formula on left ventricle. Significantly reduced TUNEL-positive cells and mitochondria- dependent apoptosis were observed in the left ventricle of hamsters from Li-Fu formula group compared to the Cholesterol group. Additionally, induced cardiac insulin like growth factor I receptor (IGFIR)-dependent survival pathway was detected in the Li-Fu formula group compared to the Cholesterol group. Besides, minor fibrosis, increased collagen deposition, and myofibril disarray was detected in the Cholesterol group, whereas the reductions of collagen deposition and myofibril disarray were observed in the Li-Fu formula group. This study demonstrated that Li-Fu formula not only reduced the mitochondria-dependent apoptosis and fibrosis, but also enhanced the IGF-I survival pathway in the left ventricle from high cholesterol-fed hamsters. We suggest the protective effects of Li-Fu formula on cardiac apoptosis and therapeutic potentials against cardiovascular disease. Hindawi Publishing Corporation 2011 2011-02-17 /pmc/articles/PMC3135794/ /pubmed/19939950 http://dx.doi.org/10.1093/ecam/nep182 Text en Copyright © 2011 Wei-Wen Kuo 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 Original Article
Kuo, Wei-Wen
Hsu, Tsai-Ching
Chain, Mei-Haung
Lai, Chao-Hung
Wang, Wen-Hong
Tsai, Fuu-Jen
Tsai, Chang-Hai
Wu, Chieh-His
Huang, Chih-Yang
Tzang, Bor-Show
Attenuated Cardiac Mitochondrial-Dependent Apoptotic Effects by Li-Fu Formula in Hamsters Fed with a Hypercholesterol Diet
title Attenuated Cardiac Mitochondrial-Dependent Apoptotic Effects by Li-Fu Formula in Hamsters Fed with a Hypercholesterol Diet
title_full Attenuated Cardiac Mitochondrial-Dependent Apoptotic Effects by Li-Fu Formula in Hamsters Fed with a Hypercholesterol Diet
title_fullStr Attenuated Cardiac Mitochondrial-Dependent Apoptotic Effects by Li-Fu Formula in Hamsters Fed with a Hypercholesterol Diet
title_full_unstemmed Attenuated Cardiac Mitochondrial-Dependent Apoptotic Effects by Li-Fu Formula in Hamsters Fed with a Hypercholesterol Diet
title_short Attenuated Cardiac Mitochondrial-Dependent Apoptotic Effects by Li-Fu Formula in Hamsters Fed with a Hypercholesterol Diet
title_sort attenuated cardiac mitochondrial-dependent apoptotic effects by li-fu formula in hamsters fed with a hypercholesterol diet
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3135794/
https://www.ncbi.nlm.nih.gov/pubmed/19939950
http://dx.doi.org/10.1093/ecam/nep182
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