Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2025
DIA proteomic analysis revealed the molecular characteristics of aluminum-induced hippocampal injury in rats.
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Liu Congying, Shi Yue, Hu Qian, Chu Yafen, Guo Yue, Song Chaoran, Jia Jingjing, He Chanting
Аннотация
BACKGROUND: Aluminum is widely used in production and daily life due to its excellent properties. However, aluminum can damage neurons and cause cognitive impairment. Therefore, studying the neurotoxic mechanism of aluminum is of great significance.
OBJECTIVE: This study established a subchronic aluminum exposure model in Sprague Dawley rats and systematically investigated the neurotoxic effects and molecular mechanisms of aluminum.
METHODS: The experimental animals were randomly divided into a control group (0.9 % saline) and an aluminum exposure group ﹛20 μmol/kg maltol aluminum [Al(mal)3]﹜. Both groups were given intraperitoneal injections every other day for 90 days. After the administration, the rats received a series of behavioral tests. Subsequently, the rat hippocampus was subjected to data independent acquisition proteomic sequencing.
RESULT: Through Morris water maze and electron microscopy analysis of hippocampal tissue, it was confirmed that rats exposed to aluminum exhibited significant learning and memory impairments, accompanied by hippocampal neuron damage. The bioinformatics results showed that 188 differentially expressed proteins were screened out. And aluminum exposure mainly damages mitochondrial function (such as oxidative phosphorylation and ATP synthesis). It is worth noting that pathway enrichment analysis suggests a common pathogenic mechanism between aluminum induced neurotoxicity and Alzheimer's disease.
CONCLUSION: This study confirms that subchronic aluminum exposure leads to cognitive decline by mediating a large amount of protein expression dysregulation. The core mechanism is to impair mitochondrial energy metabolism and synaptic plasticity.
OBJECTIVE: This study established a subchronic aluminum exposure model in Sprague Dawley rats and systematically investigated the neurotoxic effects and molecular mechanisms of aluminum.
METHODS: The experimental animals were randomly divided into a control group (0.9 % saline) and an aluminum exposure group ﹛20 μmol/kg maltol aluminum [Al(mal)3]﹜. Both groups were given intraperitoneal injections every other day for 90 days. After the administration, the rats received a series of behavioral tests. Subsequently, the rat hippocampus was subjected to data independent acquisition proteomic sequencing.
RESULT: Through Morris water maze and electron microscopy analysis of hippocampal tissue, it was confirmed that rats exposed to aluminum exhibited significant learning and memory impairments, accompanied by hippocampal neuron damage. The bioinformatics results showed that 188 differentially expressed proteins were screened out. And aluminum exposure mainly damages mitochondrial function (such as oxidative phosphorylation and ATP synthesis). It is worth noting that pathway enrichment analysis suggests a common pathogenic mechanism between aluminum induced neurotoxicity and Alzheimer's disease.
CONCLUSION: This study confirms that subchronic aluminum exposure leads to cognitive decline by mediating a large amount of protein expression dysregulation. The core mechanism is to impair mitochondrial energy metabolism and synaptic plasticity.