科研之友
微信
新浪微博
Facebook
分享链接
摘要
Aluminum (Al) is a recognized environmental pollutant that causes neuroinflammatory lesions, leading to neurodegenerative diseases. Interleukin-1 (IL-1) signaling pathway is responsible for regulating inflammatory lesions. However, it remains unclear whether IL-1 signaling pathway is involved in neuroinflammatory lesions induced by Al exposure. In the present study, one hundred and twenty Wistar rats were orally exposed to 0, 50, 150 and 450 mg/kg BW/d aluminum trichloride (AlCl3) for 90 days, respectively. We found that AlCl3 exposure increased hippocampal Al concentration, reduced hippocampus coefficient, impaired cognitive ability, deteriorated microstructure of hippocampal CA1 and CA3 regions, increased reactive oxygen species (ROS) level, activated astrocytes and microglia, increased pro-inflammatory cytokines contents and mRNA expressions, and decreased anti-inflammatory cytokines contents and mRNA expressions in the hippocampus. These results indicated that AlCl3 induced the hippocampal inflammatory lesion (HIL). Moreover, AlCl3 exposure increased the mRNA and protein expression of IL-1 signaling pathway core components in the hippocampus, demonstrating that AlCl3 activated IL-1 signaling pathway. Furthermore, the correlation between interleukin-1 beta (IL-1 beta) content and HIL and activation of the IL-1 signaling pathway was analyzed. Results showed that IL-1 beta content was positively correlated with pro-inflammatory cytokines contents and mRNA expressions and activation of IL-1 signaling pathway, and was negatively correlated with hippocampus coefficient, anti-inflammatory cytokines contents and mRNA expressions, and the number of hippocampal neurons. The above results demonstrate that AlCl3-induced HIL is associated with IL-1 signaling pathway, in which IL-1 beta is a link.
- 出版日期2018-7
- 单位东北农业大学
