期刊
CNS NEUROSCIENCE & THERAPEUTICS
卷 27, 期 7, 页码 842-856出版社
WILEY
DOI: 10.1111/cns.13645
关键词
galectin-1; IRAK1; microglia activation; neuroinflammation; perioperative neurocognitive disorders
资金
- Natural Science Foundation of Guangdong Province, China [2016A030313827, 2018A0303130272]
- Science and Technology Planning Project of Guangzhou, China [201707010207]
The study showed that galectin-1 attenuated cognitive dysfunction induced by surgery in aged mice by inhibiting microglial activity and reducing inflammatory protein expression. Galectin-1 also prevented neuronal loss in the hippocampus and inhibited inflammation in microglial cells, suggesting its potential protective effects on surgery-induced neuroinflammation.
Introduction The incidence of perioperative neurocognitive disorders (PND) is higher in the elderly patients undergoing surgery. Microglia activation-mediated neuroinflammation is one of the hallmarks of PND. Galectin-1 has been identified as a pivotal modulator in the central nervous system (CNS), while the role of galectin-1 in PND induced by microglia-mediated neuroinflammation is still undetermined. Methods An exploratory laparotomy model anesthetized with isoflurane was employed to investigate the role of galectin-1 on PND in aged mice. Open field test and Morris water maze were used to test the cognitive function 3- or 7-days post-surgery. The activation of microglia in the hippocampus of aged mice was tested by immunohistochemistry. Western blot, enzyme-linked immunosorbent assay (ELISA), and quantitative real-time polymerase chain reaction (qRT-PCR) were employed to elucidate the underlying mechanisms. Results Galectin-1 attenuated the cognitive dysfunction induced by surgery in aged mice and inhibited microglial activity. Moreover, galectin-1 decreased the expression level of inflammatory proteins (interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha), and prevented neuronal loss in the hippocampus. Galectin-1 inhibited the inflammation of BV2 microglial cells induced by lipopolysaccharide via decreasing the translocation of NF-kappa B p65 and c-Jun, while this kind of inhibition was rescued when overexpressing IRAK1. Conclusion Our findings provide evidence that galectin-1 may inhibit IRAK1 expression, thus suppressing inflammatory response, inhibiting neuroinflammation, and improving ensuing cognitive dysfunction. Collectively, these findings unveil that galectin-1 may elicit protective effects on surgery-induced neuroinflammation and neurocognitive disorders.
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