Document Detail


Preclinical evaluation of targeting the Nrf2 pathway by triterpenoids (CDDO-Im and CDDO-Me) for protection from LPS-induced inflammatory response and reactive oxygen species in human peripheral blood mononuclear cells and neutrophils.
MedLine Citation:
PMID:  17822364     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Sepsis is characterized by an inappropriate host immune-inflammatory response and sustained oxidative damage. Nrf2, a bZIP oxidant-responsive transcription factor, regulates a battery of cytoprotective genes including antioxidants and maintains cellular redox homeostasis. Mouse studies have demonstrated a critical role of Nrf2 in improving survival during sepsis. This preclinical ex vivo study using neutrophils and peripheral blood mononuclear cells (PBMCs) as a surrogate cells evaluates the efficacy of CDDO-Im and CDDO-Me [imidazole and methyl ester derivative of 2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oic acid (CDDO)] to activate the Nrf2 pathway and protect from lipopolysaccharide (LPS)-induced inflammatory response in humans. CDDO-Im treatment significantly induced Nrf2-dependent antioxidative genes (HO-1, GCLC, GCLM, and NQO1) in PBMCs isolated from six normal subjects. CDDO-Im increased nuclear accumulation of Nrf2 protein. Pretreatment of PBMC by CDDO-Im significantly attenuated LPS-induced cytokine expression. Similar increases in levels of antioxidant genes and suppression of LPS-induced cytokine expression was observed after CDDO-Me pretreatment. CDDO-Im also greatly inhibited LPS, fMLP, TNF-alpha, and TPA-induced ROS generation in neutrophils. In conclusion, these results demonstrate that activation of the Nrf2-dependent antioxidative pathway by CDDO-Im or CDDO-Me protects against the LPS-induced inflammatory response and suggest that they can be potential therapeutic candidates for intervening sepsis syndrome.
Authors:
Rajesh K Thimmulappa; Ralph J Fuchs; Deepti Malhotra; Catherine Scollick; Kassim Traore; Jay H Bream; Michael A Trush; Karen T Liby; Michael B Sporn; Thomas W Kensler; Shyam Biswal
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Publication Detail:
Type:  Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Antioxidants & redox signaling     Volume:  9     ISSN:  1523-0864     ISO Abbreviation:  Antioxid. Redox Signal.     Publication Date:  2007 Nov 
Date Detail:
Created Date:  2007-10-22     Completed Date:  2007-12-07     Revised Date:  2011-08-01    
Medline Journal Info:
Nlm Unique ID:  100888899     Medline TA:  Antioxid Redox Signal     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1963-70     Citation Subset:  IM    
Affiliation:
Department of Environmental Health Sciences, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland 21205, USA.
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MeSH Terms
Descriptor/Qualifier:
Cytokines / metabolism*
Drug Evaluation, Preclinical
Gene Expression Regulation / drug effects
Humans
Imidazoles / pharmacology*
Inflammation / chemically induced,  genetics,  immunology
Leukocytes, Mononuclear / drug effects,  immunology*
Lipopolysaccharides / toxicity
NF-E2-Related Factor 2 / genetics,  physiology*
Neutrophils / drug effects,  immunology*
Oleanolic Acid / analogs & derivatives*,  pharmacology
RNA, Messenger / metabolism
Reactive Oxygen Species / metabolism
Receptors, Formyl Peptide / metabolism
Time Factors
Tumor Necrosis Factor-alpha / metabolism
Grant Support
ID/Acronym/Agency:
CA78814/CA/NCI NIH HHS; CA94076/CA/NCI NIH HHS; GM079239/GM/NIGMS NIH HHS; HL081205/HL/NHLBI NIH HHS; P30 ES 03819/ES/NIEHS NIH HHS; P50 CA058184/CA/NCI NIH HHS; R01 GM079239-01A1/GM/NIGMS NIH HHS; R01 HL081205-03/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/1-(2-cyano-3,12-dioxooleana-1,9-dien-28-oyl) imidazole; 0/Cytokines; 0/Imidazoles; 0/Lipopolysaccharides; 0/NF-E2-Related Factor 2; 0/RNA, Messenger; 0/Reactive Oxygen Species; 0/Receptors, Formyl Peptide; 0/Tumor Necrosis Factor-alpha; 0/methyl 2-cyano-3,12-dioxoolean-1,9-dien-28-oate; 508-02-1/Oleanolic Acid
Comments/Corrections

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