title: HSF1 and NF-κB p65 participate in the process of exercise preconditioning attenuating pressure overload-induced pathological cardiac hypertrophy.
abstract: 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.
authors: Department of Cardiothoracic Surgery, No. 401 Hospital of PLA, Qingdao, China; Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China.
authors: Tongyi
authors: T
authors: Xu
authors: Centre of Cardiovascular Surgery, Guangzhou General Hospital of Guangzhou Military Region, Guangzhou, China; Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China.
authors: Ben
authors: B
authors: Zhang
authors: Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China.
authors: Fan
authors: F
authors: Yang
authors: Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China.
authors: Chengliang
authors: C
authors: Cai
authors: Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China.
authors: Guokun
authors: G
authors: Wang
authors: Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China. Electronic address: handoctor@gmail.com.
authors: Qingqi
authors: Q
authors: Han
authors: Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China. Electronic address: zouliangjiansh@gmail.com.
authors: Liangjian
authors: L
authors: Zou
mesh_terms: D000818:Animals; D001483:Base Sequence; D006332:Cardiomegaly / Q000378:metabolism* / Q000503:physiopathology; D017931:DNA Primers; D004268:DNA-Binding Proteins / Q000502:physiology*; D000076249:Heat Shock Transcription Factors; D008297:Male; D010805:Physical Conditioning, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D051996:Transcription Factor RelA / Q000502:physiology*; D014157:Transcription Factors / Q000502:physiology*
chemical_list: D017931:DNA Primers; D004268:DNA-Binding Proteins; D000076249:Heat Shock Transcription Factors; C000619709:Hsf1 protein, rat; C498145:Rela protein, rat; D051996:Transcription Factor RelA; D014157:Transcription Factors
keywords: Exercise preconditioning; HSF1; NF-κB p65; Pathological cardiac hypertrophy; Pressure-overload