Document Detail


Paeonol Attenuates Microglia-Mediated Inflammation and Oxidative Stress-Induced Neurotoxicity in Rat Primary Microglia and Cortical Neurons.
MedLine Citation:
PMID:  22089194     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
ABSTRACT: Inflammation and oxidative stress play important roles in the pathogenesis of neurodegenerative disorders such as stroke, traumatic injury, Parkinson's disease and Alzheimer's disease. Paeonol, a natural compound extracted from Moutan Cortex, is a potent anti-inflammatory and anti-oxidative agent. The aim of this study was to investigate the neuroprotective mechanisms of paeonol on lipopolysaccharides (LPS)-induced inflammation in rat primary microglia and 6-hydroxydopamine (6-OHDA)-induced oxidative damage in cortical neurons. In LPS-treated microglia, paeonol attenuated the overexpression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), leading to the decrease of nitric oxide (NO) and prostaglandin E2 (PGE2) production, respectively. Paeonol also suppressed LPS-induced phosphorylation of extracellular signal-regulated kinase (ERK), and Jun N-terminal kinase (JNK). In addition, LPS-stimulated NADPH oxidase activation, and reactive oxygen species (ROS) production were attenuated by paeonol. Paeonol-induced upregulation of heme oxygenase-1 (HO-1) was also observed. Moreover, paeonol attenuated LPS-treated microglia culture medium (LCM)-induced neuron cells death. Post-treatment with paeonol also reduced inflammatory responses in LPS-activated microglia and increased cell viability in LCM-treated neurons. Furthermore, in 6-OHDA-treated cortical neurons, paeonol not only decreased ROS production but also increased cell viability, superoxide dismutase (SOD) activity and the anti-apoptotic protein B-cell lymphoma-2 (Bcl-2) expression. Taken together, the present results suggest that paeonol might be a potential neuroprotective agent via inhibiting microglia-mediated inflammation and oxidative stress-induced neuronal damage.
Authors:
Yu-Ting Tseng; Ya-Yun Hsu; Yu-Tzu Shih; Yi-Ching Lo
Related Documents :
3134064 - Tumor necrosis factor induces tissue factor-like activity in human leukemia cell line u...
16164824 - Dexamethasone -induced apoptosis of human monocytes exposed to immune complexes. interv...
21930594 - Aryl hydrocarbon receptor negatively regulates lps-induced il-6 production through supp...
2687984 - Cell-mediated immune response in psoriasis and psoriatic arthritis.
1387284 - Effects of the immunomodulator diacetyl-splenopentin on antigen-induced arthritis in ra...
7094424 - C3b inactivator deficiency with immune complex manifestations.
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-11-15
Journal Detail:
Title:  Shock (Augusta, Ga.)     Volume:  -     ISSN:  1540-0514     ISO Abbreviation:  -     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2011-11-17     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9421564     Medline TA:  Shock     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
*Graduate Institute of Natural Products, †Graduate Institute of Medicine and ‡Department of Pharmacology, Kaohsiung Medical University, Kaohsiung 80708, Taiwan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Increased Granzyme Levels in Cytotoxic T Lymphocytes are Associated with Disease Severity in Emergen...
Next Document:  Acute Effects of Balanced vs Unbalanced Colloid Resuscitation on Renal Macro- and Microcirculatory P...