HSF1 and NF-κB p65 participate in the process of exercise preconditioning attenuating pressure overload-induced pathological cardiac hypertrophy
Autor: | Ben Zhang, Chengliang Cai, Qingqi Han, Liangjian Zou, Fan Yang, Guokun Wang, Tongyi Xu |
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Rok vydání: | 2015 |
Předmět: |
Male
medicine.medical_specialty Central nervous system Biophysics Ischemia Cardiomegaly Real-Time Polymerase Chain Reaction Biochemistry Muscle hypertrophy Rats Sprague-Dawley Heat Shock Transcription Factors Downregulation and upregulation Physical Conditioning Animal Internal medicine Heat shock protein medicine Animals Myocyte Molecular Biology DNA Primers Pressure overload Base Sequence business.industry Transcription Factor RelA Cell Biology medicine.disease Rats Hsp70 DNA-Binding Proteins stomatognathic diseases Endocrinology medicine.anatomical_structure business Transcription Factors |
Zdroj: | Biochemical and Biophysical Research Communications. 460:622-627 |
ISSN: | 0006-291X |
DOI: | 10.1016/j.bbrc.2015.03.079 |
Popis: | Pathological cardiac hypertrophy, often accompanied by hypertension, aortic stenosis and valvular defects, is typically associated with myocyte remodeling and cardiac dysfunction. Exercise preconditioning (EP) has been proven to enhance the tolerance of the myocardium to cardiac ischemia-reperfusion injury. However, the effects of EP in pathological cardiac hypertrophy are rarely reported. 10-wk-old male Sprague-Dawley rats (n = 80) were randomly divided into four groups: sham, TAC, EP + sham and EP + TAC. Two EP groups were subjected to 4 weeks of treadmill training, and the EP + TAC and TAC groups were followed by TAC operations. The sham and EP + sham groups underwent the same operation without aortic constriction. Eight weeks after the surgery, we evaluated the effects of EP by echocardiography, morphology, and histology and observed the expressions of the associated proteins. Compared with the respective control groups, hypertrophy-related indicators were significantly increased in the TAC and EP + TAC groups (p < 0.05). However, between the TAC and EP + TAC groups, all of these changes were effectively inhibited by EP treatment (p < 0.05). Furthermore, EP treatment upregulated the expression of HSF1 and HSP70, increased the HSF1 levels in the nuclear fraction, inhibited the expression of the NF-κB p65 subunit, decreased the NF-κB p65 subunit levels in the nuclear fraction, and reduced the IL2 levels in the myocardia of rats. EP could effectively reduce the cardiac hypertrophic responses induced by TAC and may play a protective role by upregulating the expressions of HSF1 and HSP70, activating HSF1 and then inhibiting the expression of NF-κB p65 and nuclear translocation. |
Databáze: | OpenAIRE |
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