Glial activation with concurrent up-regulation of inflammatory mediators in trimethyltin-induced neurotoxicity in mice
- Glial activation with concurrent up-regulation of inflammatory mediators in trimethyltin-induced neurotoxicity in mice
- 김주환; 양미영; 손영훈; 장효선; 김동우; 김종춘; 김성호; 강만종; 임혜인; 신태균; 문창종
- Trimethyltin; Hippocampus; Neuroinflammation; Glial activation; Cytokine
- Issue Date
- Acta histochemica
- VOL 116, NO 8, 1490-1500
- 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.
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