SIRT1 is a regulator in high glucose-induced inflammatory response in RAW264.7 cells.
SIRT1 is a regulator in high glucose-induced inflammatory response in RAW264.7 cells.
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DOI：
10.1371/journal.pone.0120849
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发表时间：
2015
期刊：
影响因子：
3.7
通讯作者：
Hu D
中科院分区：
文献类型：
--
作者：
Jia Y;Zheng Z;Wang Y;Zhou Q;Cai W;Jia W;Yang L;Dong M;Zhu X;Su L;Hu D
脓毒症被定义为一种全身性炎症反应综合征，其破坏宿主免疫系统的功能，包括免疫巨噬细胞介导的促炎反应和抗炎反应之间的不平衡。脓毒症还可能诱发急性高血糖。研究表明，沉默交配型信息调节 2 同源物 1 (SIRT1) 是一种 NAD+ 依赖性脱乙酰酶，可介导 NF-κb 脱乙酰化并抑制其功能。因此，SIRT1很可能在高糖介导的炎症信号传导中发挥重要作用。在这里，我们证明高葡萄糖显着下调 RAW264.7 巨噬细胞中 SIRT1 的 mRNA 和蛋白质水平，并上调 mRNA 水平和两种促炎细胞因子 IL-1β 和 TNF-α 的释放。有趣的是，SIRT1 激活剂 SRT1720 显着上调了高葡萄糖导致的 SIRT1 水平降低，而 IL-1β 和 TNF-α 的水平和释放随着 SRT1720 的使用而显着降低。然而，当SIRT1的功能被EX527抑制或其表达被RNAi抑制时，高糖引起的IL-1β和TNF-α的上调水平和释放进一步增加。总而言之，这些发现共同表明 SIRT1 是许多高血糖相关炎症性疾病（例如脓毒症）的重要调节因子。
Sepsis is defined as a systemic inflammatory response syndrome that disorders the functions of host immune system, including the imbalance between pro- and anti-inflammatory responses mediated by immune macrophages. Sepsis could also induce acute hyperglycemia. Studies have shown that the silent mating type information regulation 2 homolog 1 (SIRT1), an NAD+-dependent deacetylase, mediates NF-κb deacetylation and inhibits its function. Therefore, SIRT1 is likely to play an important role in high glucose-mediated inflammatory signalings. Here we demonstrate that high glucose significantly downregulates both the mRNA and protein levels of SIRT1 and upregulates the mRNA level and the release of two pro-inflammatory cytokines, IL-1β and TNF-α, in RAW264.7 macrophages. Interestingly, the reduced level of SIRT1 by high glucose is remarkably upregulated by SIRT1 activator SRT1720, while the level and the release of IL-1β and TNF-α significantly decrease with the use of SRT1720. However, when the function of SIRT1 is inhibited by EX527 or its expression is suppressed by RNAi, the upregulated level and release of IL-1β and TNF-α by high glucose are further increased. Taken together, these findings collectively suggest that SIRT1 is an important regulator in many high glucose-related inflammatory diseases such as sepsis.
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影响因子：
3.7
作者：
Mortuza R;Chen S;Feng B;Sen S;Chakrabarti S
通讯作者：
Chakrabarti S
影响因子：
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作者：
Yang HH;Huang FF;Lai YH;Yang HJ;Yu JC
通讯作者：
Yu JC
影响因子：
4.8
作者：
Liu, Tie Fu;Yoza, Barbara K.;Mccall, Charles E.
通讯作者：
Mccall, Charles E.
DOI：
10.1016/j.bbrc.2012.09.042
发表时间：
2012-10-12
影响因子：
3.1
作者：
Takeda-Watanabe, Ai;Kitada, Munehiro;Koya, Daisuke
通讯作者：
Koya, Daisuke
DOI：
10.1152/ajpendo.00530.2010
发表时间：
2011-11-01
影响因子：
5.1
作者：
Centeno-Baez, Carolina;Dallaire, Patrice;Marette, Andre
通讯作者：
Marette, Andre