학술논문

High dietary taurine inhibits myocardial apoptosis during an atherogenic diet: association with increased myocardial HSP70 and HSF-1 but not caspase 3.
Document Type
Article
Source
European Journal of Nutrition. Apr2014, Vol. 53 Issue 3, p929-937. 9p.
Subject
*AMINO acid metabolism
*PROTEIN metabolism
*CYSTEINE metabolism
*METHIONINE metabolism
*ANALYSIS of variance
*ANIMAL experimentation
*APOPTOSIS
*ATHEROSCLEROSIS
*BIOPHYSICS
*COMPARATIVE studies
*DIETARY supplements
*FAT content of food
*HISTOLOGICAL techniques
*IMMUNOHISTOCHEMISTRY
*RESEARCH methodology
*MYOCARDIUM
*RABBITS
*RESEARCH funding
*STATISTICS
*WESTERN immunoblotting
*HOMOCYSTEINE
*DATA analysis
*OXIDATIVE stress
*SULFUR acids
*DESCRIPTIVE statistics
Language
ISSN
1436-6207
Abstract
Background and aim: Apoptosis is a major cause of myocyte death, and taurine is anti-apoptotic. Heat shock protein 70 (HSP70) (which is regulated by heat shock factor-HSF-1) is also anti-apoptotic, and caspase 3 stimulates the apoptotic pathway. This study investigated whether taurine affects atherogenic diet-induced myocardial apoptosis, and whether HSP70, HSF-1 and caspase 3 are involved. Methods: New Zealand white rabbits were divided into 3 groups for 4 weeks according to their diet. Group 1 (control) was fed a normal rabbit diet; Group 2 (MC) received a normal rabbit diet with 1 % methionine plus 0.5 % cholesterol. Group 3 received MC diet + 2.5 % taurine (MCT). Results: The atherogenic diet did not affect myocardial HSP70 or HSF-1 protein, but increased myocardial apoptotic nuclei to 40 % ( p < 0.01) versus 7 % in con and 12 % in MCT ( p < 0.01). However, in MCT, myocardial HSP70 expression increased by 42.7 % versus con and MC ( p = 0.016), HSF-1 by 12 % versus con and MC ( p < 0.05), and total nuclei count increased by 37 % versus MC ( p < 0.05). Caspase 3 subunits remained unchanged in all groups, and HSP70 was increased approximately twofold in endothelial layer of arterioles ( p = 0.01). Conclusion: This study shows that taurine could reduce myocardial apoptotic nuclei and thus confer myocardial cytoprotection via stimulating myocardial HSP70 via HSF-1 and caspase 3-independent mechanisms. [ABSTRACT FROM AUTHOR]