Glial activation with concurrent up-regulation of inflammatory mediators in trimethyltin-induced neurotoxicity in mice

Title
Glial activation with concurrent up-regulation of inflammatory mediators in trimethyltin-induced neurotoxicity in mice
Authors
김주환양미영손영훈장효선김동우김종춘김성호강만종임혜인신태균문창종
Keywords
Trimethyltin; Hippocampus; Neuroinflammation; Glial activation; Cytokine
Issue Date
2014-10
Publisher
Acta histochemica
Citation
VOL 116, NO 8, 1490-1500
Abstract
Trimethyltin (TMT), a potent neurotoxic chemical, causes dysfunction and neuroinflammation in thebrain, particularly in the hippocampus. The present study assessed TMT-induced glial cell activationand inflammatory cytokine alterations in the mouse hippocampus, BV-2 microglia, and primary cul-tured astrocytes. In the mouse hippocampus, TMT treatment significantly increased the expression ofglial cell markers, including the microglial marker ionized calcium-binding adapter molecule 1 and theastroglial marker glial fibrillary acidic protein. The expression of M1 and M2 microglial markers (induciblenitric oxide synthase [iNOS] and CD206, respectively) and pro-inflammatory cytokines (interleukin [IL]-1β , IL-6 and tumor necrosis factor [TNF]- α) were significantly increased in the mouse hippocampusfollowing TMT treatment. In BV-2 microglia, iNOS, IL-1 β, TNF-α , and IL-6 expression increased sig-nificantly, whereas arginase-1 and CD206 expression decreased significantly after TMT treatment in atime- and concentration-dependent manner. In primary cultured astrocytes, iNOS, arginase-1, IL-1β ,TNF-α , and IL-6 expression increased significantly, whereas IL-10 expression decreased significantlyafter TMT treatment in a time- and concentration-dependent manner. These results indicate that signif-icant up-regulation of pro-inflammatory signals in TMT-induced neurotoxicity may be associated withpathological processing of TMT-induced neurodegeneration.
URI
http://pubs.kist.re.kr/handle/201004/48848
ISSN
00651281
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KIST Publication > Article
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