神经炎症
内科学
内分泌学
后代
齿状回
促炎细胞因子
过氧化物酶体增殖物激活受体
十六酰胺乙醇
生物
小胶质细胞
谷胱甘肽过氧化物酶
海马结构
受体
超氧化物歧化酶
氧化应激
兴奋剂
医学
炎症
大麻素受体
遗传学
怀孕
作者
Wen‐Chung Liu,Chih‐Wei Wu,Mu‐Hui Fu,You‐Lin Tain,Chih‐Kuang Liang,Chun‐Ying Hung,I‐Chun Chen,Yu‐Chi Lee,Cai-Yi Wu,Kou-Juey Wu
标识
DOI:10.1016/j.jnutbio.2020.108378
摘要
The mechanisms beneath the initiation of neuroinflammation are still inconclusive. Growing evidence proposes the maternal effect on the development of neuroinflammation. In this study, we evaluated the upstream regulators and the indices of neuroinflammation in the hippocampi of female offspring at 3 months old. The accumulation of nuclear factor-κB (NF-κB, 65 kDa), a cytokine-encoding transcription factor, was increased in microglia. The enhanced microglial activation was detected in CA1, CA3 and dentate gyrus (DG) HFD group with upregulation of CD11b and ionized calcium binding adaptor molecule 1 (Iba-1). Moreover, proinflammatory cytokines (including TNFα, IL-1β and IL-6) were significantly increased in HFD group. Peroxisome proliferator-activated receptors γ (PPARγ) is a transcription factor involved in the suppression of NF-κB expression and in encoding endogenous antioxidants (such as catalase and glutathione peroxidases). On the contrary, the expression of nuclear PPARγ was suppressed in hippocampal neurons of the HFD group. In addition, the expressions of glutathione peroxidase 1 (GPx1) was suppressed in HFD group. Oral application with pioglitazone, a PPARγ agonist, effectively ceased the neuroinflammation and reversed the expression of antioxidants in HFD group. Together, these results for the first time demonstrated that maternal HFD triggered the waxing and waning of NF-κB and PPARγ may initiate neuroinflammation in the hippocampus of adult female offspring. Our findings further suggest that PPARγ could be the feasible targets to reprogram the hippocampal impairment induced by maternal HFD.
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