Adjudin attenuates lipopolysaccharide (LPS)- and ischemia-induced microglial activation

Abstract Neuroinflammation caused by microglial activation plays a key role in ischemia, neurodegeneration and many other CNS diseases. In this study, we found that Adjudin, a potential non-hormonal male contraceptive, exhibits additional function to reduce the production of proinflammatory mediator...

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Bibliographic Details
Published in:Journal of neuroimmunology 2013-01, Vol.254 (1), p.83-90
Main Authors: Shao, Jiaxiang, Liu, Tengyuan, Xie, Qian Reuben, Zhang, Tingting, Yu, Hemei, Wang, Boshi, Ying, Weihai, Mruk, Dolores D, Silvestrini, Bruno, Yan Cheng, C, Xia, Weiliang
Format: Article
Language:English
Subjects:
Adjudin
Allergy and Immunology
Analysis of Variance
Animals
Anti-Inflammatory Agents - therapeutic use
Brain edema
Brain Edema - etiology
Brain Edema - prevention & control
Brain Infarction - etiology
Brain Infarction - prevention & control
CD11b Antigen - metabolism
Cell Line, Transformed
Cell Survival - drug effects
Cytokine
Disease Models, Animal
Dose-Response Relationship, Drug
Drug Interactions
Hydrazines - therapeutic use
Indazoles - therapeutic use
Infarction, Middle Cerebral Artery - complications
Infarction, Middle Cerebral Artery - drug therapy
Infarction, Middle Cerebral Artery - pathology
Lipopolysaccharides - toxicity
Male
Mice
Mice, Inbred ICR
Microglia - drug effects
Microglial activation
Nervous System Diseases - drug therapy
Nervous System Diseases - etiology
Neurology
NF-kappa B - metabolism
NF-κB
Psychomotor Performance - drug effects
Signal Transduction - drug effects
Time Factors
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Summary:Abstract Neuroinflammation caused by microglial activation plays a key role in ischemia, neurodegeneration and many other CNS diseases. In this study, we found that Adjudin, a potential non-hormonal male contraceptive, exhibits additional function to reduce the production of proinflammatory mediators. Adjudin significantly inhibited LPS-induced IL-6 release and IL-6, IL-1β, TNF-α expression in BV2 microglial cells. Furthermore, Adjudin exhibited anti-inflammatory properties by suppression of NF-κB p65 nuclear translocation and DNA binding activity as well as ERK MAPK phosphorylation. To determine the in vivo effect of Adjudin, we used a permanent middle cerebral artery occlusion (pMCAO) mouse model and found that Adjudin could reduce ischemia-induced CD11b expression, a marker of microglial activation. Furthermore, Adjudin treatment attenuated brain edema and neurological deficits after ischemia but did not reduce infarct volume. Thus, our data suggest that Adjudin may be useful for mitigating neuroinflammation.
ISSN:0165-5728
1872-8421
DOI:10.1016/j.jneuroim.2012.09.012