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

作者：Kim Juhwan; Yang Miyoung; Son Yeonghoon; Jang Hyosun; Kim Dongwoo; Kim Jong Choon; Kim Sung Ho; Kang Man Jong; Im Heh In; Shin Taekyun^*; Moon Changjong

来源：Acta Histochemica, 2014, 116(8): 1490-1500.

DOI：10.1016/j.acthis.2014.09.003

• Trimethyltin
• Hippocampus
• Neuroinflammation
• Glial activation
• Cytokine

Trimethyltin (TMT), a potent neurotoxic chemical, causes dysfunction and neuroinflammation in the brain, particularly in the hippocampus. The present study assessed TMT-induced glial cell activation and inflammatory cytokine alterations in the mouse hippocampus, BV-2 microglia, and primary cultured astrocytes. In the mouse hippocampus, TMT treatment significantly increased the expression of glial cell markers, including the microglial marker ionized calcium-binding adapter molecule 1 and the astroglial marker glial fibrillary acidic protein. The expression of M1 and M2 microglial markers (inducible nitric oxide synthase [NOS] and CD206, respectively) and pro-inflammatory cytokines (interleukin [IL]-1 beta, IL-6 and tumor necrosis factor [TNF]-alpha) were significantly increased in the mouse hippocampus following TMT treatment. In BV-2 microglia, iNOS, IL-beta, TNF-alpha, and IL-6 expression increased significantly, whereas arginase-1 and CD206 expression decreased significantly after TMT treatment in a time- and concentration-dependent manner. In primary cultured astrocytes, iNOS, arginase-1, TNF-alpha, and IL-beta expression increased significantly, whereas IL-10 expression decreased significantly after TMT treatment in a time- and concentration-dependent manner. These results indicate that significant up-regulation of pro-inflammatory signals in TMT-induced neurotoxicity may be associated with pathological processing of TMT-induced neurodegeneration.

• 出版日期2014