期刊
BRAIN RESEARCH
卷 1774, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.brainres.2021.147708
关键词
Docosahexaenoic acid; Hypoglycemia; Neuron death; Necroptosis; PPAR-gamma,neonate
资金
- Applied Basic Research Programs of Science and Technology Department of Sichuan Province [2018JY0301]
- School fund project of Chengdu Medical College [CYTD18-06]
- Sichuan Province Medical Association [S18081]
- First Affiliated Hospital of Chengdu Medical College [CYFY2018YB01]
- Chengdu Medical College Graduate Research and Innovation Fund [519-2020018]
DHA has been shown to be neuroprotective and important to neurogenesis, playing a protective role against HG-induced brain injury through the PPAR-gamma/NF-kappa B pathway.
DHA has been shown to be neuroprotective and important to neurogenesis, but its role in HG-induced brain injury and the underlying mechanisms remain unknown. To elucidate the therapeutic effect of DHA, we established a mouse model with insulin-induced hypoglycemic brain injury and an in vitro model of HT-22 cells using a sugar-free medium. DHA treatment significantly reduced neuronal death and improved HG-induced learning and memory deficits. Moreover, DHA inhibited neuronal necroptosis and decreased the concentrations of TNF-alpha, IL-1 beta and TNFR1. DHA also activated PPAR-gamma and suppressed the NF-kappa B pathway in mouse brain tissues. In vitro, DHA treatment restored the viability and decreased necroptosis of HT-22 cells treated with glucose deprivation. However, the inhibition of PPAR-gamma with T0070907 reversed neuroprotective and anti-necroptosis effects of DHA in HG-induced brain injury, which is associated with the activation of the downstream NF-kappa B pathway. We conclude that DHA displays a protective effect against HG-induced brain injury through the PPAR-gamma/NF-kappa B pathway and represents a promising method to prevent HG-induced brain injury.
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