title: [Exercise preconditioning attenuates pressure overload-induced pathological cardiac hypertrophy: potential role of HSF1 and NF-κB p65 signaling].
abstract: OBJECTIVE
  To observe the effect of exercise preconditioning (EP) on pressure overload-induced pathological cardiac hypertrophy and explore related mechanisms.
  
  
  METHODS
  Ten-week-old male Sprague-Dawley rats (n = 80) were randomly divided into four groups via random number table method: sham, TAC, EP + sham and EP + TAC. Two EP groups were subjected to 4 weeks of treadmill training, and followed by sham and TAC operations. Eight weeks after the surgery, mean arterial pressure (MAP), cardiac morphology, mRNA expressions of the B-type natriuretic peptide (BNP) and heat shock protein (HSP) 70 and protein expression of the BNP, heat shock transcription factor 1 (HSF1), HSP70, nuclear factor κB (NF-κB) p65, and interleukin-2 (IL-2) were examined.
  
  
  RESULTS
  (1) Pathological cardiac hypertrophy index: eight weeks after TAC, MAP, heart size, HW/BW, cross-sectional area of the cardiomyocytes (CSA) and mRNA and protein expressions of BNP in the LV were all significantly higher in the TAC and EP + TAC groups than respective sham groups (all P < 0.05). HW/BW, CSA, and mRNA and protein expressions of BNP in the LV were significantly lower in EP + TAC group than in TAC group (all P < 0.05). (2) mRNA and protein expressions of HSF1 and HSP70 and nuclear HSF1 levels were significantly downregulated post TAC, however, EP treatment significantly increased the expression of HSF1 and nuclear HSF1 levels in TAC rats (all P < 0.05). (3) mRNA and protein expressions of NF-κB p65 and IL-2 were significantly increased in the TAC and EP + TAC groups compared with the respective sham groups (all P < 0.05), which were significantly downregulated in EP + TAC group compared to TAC group (all P < 0.05).
  
  
  CONCLUSIONS
  EP could effectively reduce the cardiac hypertrophic responses induced by TAC possibly through upregulating the expressions of HSF1 and HSP70 and inhibiting the expression of NF-κB p65 and its nuclear translocation.
authors.affiliation: Department of Cardiothoracic Surgery, No. 401 Hospital of PLA, Qingdao 266071, China.
authors.forename: Tongyi
authors.initials: T
authors.lastname: Xu
authors.forename: Tao
authors.initials: T
authors.lastname: Li
authors.forename: Fan
authors.initials: F
authors.lastname: Yang
authors.forename: Qingqi
authors.initials: Q
authors.lastname: Han
authors.affiliation: Email: zouliangjiansh@gmail.com.
authors.forename: Liangjian
authors.initials: L
authors.lastname: Zou
mesh_terms: D000818:Animals; D006332:Cardiomegaly; D004268:DNA-Binding Proteins; D015536:Down-Regulation; D018840:HSP70 Heat-Shock Proteins; D000076249:Heat Shock Transcription Factors; D007376:Interleukin-2; D008297:Male; D032383:Myocytes, Cardiac; D020097:Natriuretic Peptide, Brain; D010805:Physical Conditioning, Animal; D012333:RNA, Messenger; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction; D051996:Transcription Factor RelA; D014157:Transcription Factors
chemical_list: D004268:DNA-Binding Proteins; D018840:HSP70 Heat-Shock Proteins; D000076249:Heat Shock Transcription Factors; C000619709:Hsf1 protein, rat; D007376:Interleukin-2; D012333:RNA, Messenger; C498145:Rela protein, rat; D051996:Transcription Factor RelA; D014157:Transcription Factors; D020097:Natriuretic Peptide, Brain