4.7 Article

Aluminum induces neuroinflammation via P2X7 receptor activating NLRP3 inflammasome pathway

期刊

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2022.114373

关键词

Aluminum; Neuroinflammation; NLRP3 inflammasome

向作者/读者索取更多资源

Aluminum exposure activates microglia and induces neuroinflammation through P2X7-NLRP3 pathway. P2X7 and HIF-1 alpha have a mutual regulatory relationship in the progression of neuroinflammation. BBG and YC-1 intervention can relieve the injuries caused by aluminum-induced neuroinflammation.
Introduction: Aluminum is everywhere in nature and is a recognized neurotoxicant closely associated with various neurodegenerative diseases. Neuroinflammation occurs in the early stage of neurodegenerative diseases, but the underlying mechanism by which aluminum induces neuroinflammation remains unclear. Material and methods: A 3-month subchronic aluminum exposure mouse model was established by drinking water containing aluminum chloride (AlCl3). Microglia BV2 cells and hippocampal neuron HT22 cells were treated with AlCl3 in vitro. BBG and YC-1 were used as intervention agents.Results: Aluminum could activate microglia and increase the level of extracellular ATP, stimulate P2X7 receptor, HIF-1 alpha, activate NLRP3 inflammasome and CASP-1, release more cytokine IL-1 beta, and induce an inflammatory response in nerve cells. There was a mutual regulatory relationship between P2X7 and HIF-1 alpha at mRNA and protein levels. The co-culture system of BV2-HT22 cells observed that conditioned medium from microglia treated with aluminum could aggravate neuronal morphological damage, inflammatory response and death. While BBG and YC-1 intervention could rescue these injuries to some extent.Conclusion: The P2X7-NLRP3 pathway was involved in aluminum-induced neuroinflammation and injury. P2X7 and HIF-1 alpha might mutually regulate and promote the progression of neuroinflammation, both BBG and YC-1 could relieve it.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.7
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据