期刊
BRAIN RESEARCH BULLETIN
卷 194, 期 -, 页码 1-12出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.brainresbull.2023.01.001
关键词
IGF2; Neuroinflammation; Microglia; Lipopolysaccharide; Depression
The role of IGF2 in modulating microglia response to neuroinflammation and its potential therapeutic effects on neuropsychiatric disorders are investigated in this study. The results showed that systemic administration of IGF2 could inhibit microglia over-activation and prevent their transformation to a pro-inflammatory phenotype, thus protecting hippocampal neurogenesis. These findings may contribute to the development of innovative therapy for neuropsychiatric disorders.
Over-activated microglia and inflammatory mediators are found in patients with depression, while manipulation of the microglia function might represent a potential therapeutic strategy. Insulin-like growth factor 2 (IGF2) has been implicated in bacterial infections and autoimmune disorders, but the role of IGF2 on the active phenotype of microglia and neuroinflammation has not been well established. IGF2 influences in modulating microglia responding to neuroinflammation induced by lipopolysaccharide(LPS)challenge will be carefully examined. In the current study, we verified that systemic IGF2 treatment could produce an anti-depression effect in LPS-treated mice. Particularly, we found that systemic IGF2 treatment inhibited microglia over-activation and pre-vented its transformation to a pro-inflammatory phenotype, thereby protecting hippocampal neurogenesis. Since microglia reactive to neuroinflammation is a common feature of neuropsychiatric disorders, the discoveries from the present study may provide therapeutic innovation for these diseases.
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