Intermittent High Glucose Exacerbates A-FABP Activation and Inflammatory Response through TLR4-JNK Signaling in THP-1 Cells.
Intermittent High Glucose Exacerbates A-FABP Activation and Inflammatory Response through TLR4-JNK Signaling in THP-1 Cells.
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间歇性高血糖通过 TLR4-JNK 信号在 THP-1 细胞中加剧 A-FABP 激活和炎症反应
DOI：
10.1155/2018/1319272
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发表时间：
2018
影响因子：
4.1
通讯作者：
Dai RP
中科院分区：
文献类型：
--
作者：
Li H;Luo HY;Liu Q;Xiao Y;Tang L;Zhong F;Huang G;Xu JM;Xu AM;Zhou ZG;Dai RP
Glucose fluctuation confers additional risks on diabetes-related vascular diseases, but the underlying mechanisms are unknown. Macrophage activation mediated by TLR4-JNK signaling plays an important role during the progress of diabetes. In the present study, we hypothesize that glucose fluctuation results in macrophage inflammation through TLR4-JNK signaling pathways. THP-1 cells were treated with normal glucose (5 mM), constant high glucose (25 mM), and intermittent high glucose (rotation per 6 h in 5 mM or 25 mM) for 24 h. The mRNA and protein expression levels of TLR4, p-JNK, and adipocyte fatty acid-binding protein (A-FABP) were determined, and the proinflammatory cytokines TNF-α and IL-1β were quantified. In constant high glucose, TLR4 expression and JNK phosphorylation levels increased, and this effect was more pronounced in intermittent high glucose. Accordingly, the expression of A-FABP and the release of the proinflammatory cytokines TNF-α and IL-1β also increased in response to constant high glucose, an effect that also was more evident in intermittent high glucose. The inhibition of p-JNK by SP600125 did not attenuate TLR4 expression, but totally inhibited both A-FABP expression and the production of the proinflammatory cytokines TNF-α and IL-1β in both constant and intermittent high glucose. Intermittent high glucose potentiates A-FABP activation and inflammatory responses via TLR4/p-JNK signaling in THP-1 cells. These findings suggest a more detrimental impact of glucose fluctuation on macrophage inflammation in diabetes-related vascular diseases than thus far generally assumed.
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影响因子：
158.5
作者：
Duckworth, William;Abraira, Carlos;Huang, Grant D.
通讯作者：
Huang, Grant D.
影响因子：
3.7
作者：
Jia Y;Zheng Z;Wang Y;Zhou Q;Cai W;Jia W;Yang L;Dong M;Zhu X;Su L;Hu D
通讯作者：
Hu D
影响因子：
16.6
作者：
Shu L;Hoo RL;Wu X;Pan Y;Lee IP;Cheong LY;Bornstein SR;Rong X;Guo J;Xu A
通讯作者：
Xu A
影响因子：
3
作者：
Hirsch, IB;Brownlee, M
通讯作者：
Brownlee, M
影响因子：
4.8
作者：
Cheng, Cheng-I;Chen, Po-Han;Kao, Ying-Hsien
通讯作者：
Kao, Ying-Hsien