Document Detail


Lipopolysaccharide pretreatment protects against ischemia/reperfusion injury via increase of HSP70 and inhibition of NF-κB.
MedLine Citation:
PMID:  21080136     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
It has been reported that pretreatment of rats with lipopolysaccharide (LPS) increases myocardial functional recovery in ischemia/reperfusion (I/R) hearts. However, the mechanisms by which LPS induces cardioprotection against I/R injury have not been fully elucidated. In this study, we pretreated rats with LPS (1.0 mg/kg) 24 h before they were subjected to I/R injury, and then examined the roles of heat shock protein-70 (HSP70) and nucleus factor-κB (NF-κB) in LPS-induced cardioprotection. We observed that pretreatment with low-dose LPS resulted in significantly increased levels of HSP70 in the myocardium, which could dramatically inhibit NF-κB translocation and reduce degradation of inhibitory κB. Inhibition of NF-κB, in turn, attenuated release of inflammatory cytokines (tumor necrosis factor-α, interleukin (IL)-1β, and IL-6) and reduced apoptosis of myocardium and infarct area following I/R injury. Moreover, HSP70 could ameliorate oxidative stress following I/R injury. To further investigate whether increase of HSP70 might be responsible for protection of the myocardium against I/R injury, we co-administered the HSP70 inhibitor, quercetin, with LPS before I/R injury. We found that LPS-induced cardioprotection was attenuated by co-administration with quercetin. Herein, we concluded that increased levels of HSP70 through LPS pretreatment led to inhibition of NF-κB activity in the myocardium after I/R injury. Our results indicated that LPS-induced cardioprotection was mediated partly through inhibition of NF-κB via increase of HSP70, and LPS pretreatment could provide a means of reducing myocardial I/R injury.
Authors:
Yong-wei Yao; Guo-hui Zhang; Ying-yu Zhang; Wei-dong Li; Cheng-hua Wang; Chun-yang Yin; Fu-min Zhang
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-11-16
Journal Detail:
Title:  Cell stress & chaperones     Volume:  16     ISSN:  1466-1268     ISO Abbreviation:  Cell Stress Chaperones     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-04-06     Completed Date:  2011-07-27     Revised Date:  2013-07-03    
Medline Journal Info:
Nlm Unique ID:  9610925     Medline TA:  Cell Stress Chaperones     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  287-96     Citation Subset:  IM    
Affiliation:
Department of Cardiology, Affiliated People's Hospital of Jiangsu University, No. 8 DianLi Road, Zhenjiang, Jiangsu, People's Republic of China. ywyao78@sina.com.cn
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / drug effects
HSP70 Heat-Shock Proteins / metabolism*
I-kappa B Proteins / metabolism
Inflammation / complications,  pathology
Lipopolysaccharides / pharmacology*
Male
Myocardium / pathology
NF-kappa B / antagonists & inhibitors*,  metabolism
Oxidative Stress / drug effects
Protein Processing, Post-Translational / drug effects
Rats
Rats, Wistar
Reperfusion Injury / complications,  metabolism*,  pathology,  prevention & control*
Chemical
Reg. No./Substance:
0/HSP70 Heat-Shock Proteins; 0/I-kappa B Proteins; 0/Lipopolysaccharides; 0/NF-kappa B
Comments/Corrections

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