| Lipopolysaccharide pretreatment protects against ischemia/reperfusion injury via increase of HSP70 and inhibition of NF-κB. | |
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MedLine Citation:
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PMID: 21080136 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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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:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-11-16 |
Journal Detail:
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Title: Cell stress & chaperones Volume: 16 ISSN: 1466-1268 ISO Abbreviation: Cell Stress Chaperones Publication Date: 2011 May |
Date Detail:
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Created Date: 2011-04-06 Completed Date: 2011-07-27 Revised Date: 2011-11-01 |
Medline Journal Info:
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Nlm Unique ID: 9610925 Medline TA: Cell Stress Chaperones Country: Netherlands |
Other Details:
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Languages: eng Pagination: 287-96 Citation Subset: IM |
Affiliation:
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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 |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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0/HSP70 Heat-Shock Proteins; 0/I-kappa B Proteins; 0/Lipopolysaccharides; 0/NF-kappa B |
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