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Fructose-1,6-bisphosphate attenuates induction of nitric oxide synthase in microglia stimulated with lipopolysaccharide

机译：1,6-二磷酸果糖减弱脂多糖刺激的小胶质细胞中一氧化氮合酶的诱导

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Aims: Fructose-1,6-bisphosphate (FBP) is a glycolytic intermediate with neuroprotective action in various brain injury models. However, the mechanism underlying the neuroprotection of FBP has not been fully defined. In this study, we investigated whether FBP inhibits endotoxin-induced nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression in microglial cells and explored the possible mechanisms of the effects of FBP. Main methods: Murine microglial cell line BV2 and primary cultured murine microglial cells were used. NO production and iNOS expression were determined by Griess reaction, RT-PCR and Western blot. Luciferase assay using iNOS promoter-luciferase (iNOS-Luc) construct was adopted for measuring transcriptional activity. Key findings: FBP dose-dependently suppressed lipopolysaccharide (LPS)-induced NO production, along with reducing the expression of iNOS at both the protein and mRNA level in primary cultured murine microglia and BV2 cells. FBP significantly inhibited iNOS promoter activity but stabilized iNOS mRNA. Among transcription factors known to be related to iNOS expression, activator protein (AP-1) activation was significantly blocked by FBP. FBP suppressed LPS-induced phosphorylation of three MAPK subtypes-p38 MAPK, JNK and ERK. FBP inhibited LPS-induced production of reactive oxygen species (ROS) and decreased intracellular GSSG/GSH ratio. Significance: Our findings suggest that FBP attenuates the LPS-induced iNOS expression through inhibition of JNK and p38 MAPK, which might be related to ROS downregulation.
机译：目的：1,6-双磷酸果糖（FBP）是在各种脑损伤模型中具有神经保护作用的糖酵解中间体。但是，尚未完全确定FBP的神经保护机制。在这项研究中，我们调查了FBP是否抑制小胶质细胞中内毒素诱导的一氧化氮（NO）的产生和诱导型一氧化氮合酶（iNOS）的表达，并探讨了FBP影响的可能机制。主要方法：使用鼠小胶质细胞系BV2和原代培养的鼠小胶质细胞。通过Griess反应，RT-PCR和Western印迹测定NO产生和iNOS表达。采用iNOS启动子-荧光素酶（iNOS-Luc）构建体的荧光素酶测定法用于测量转录活性。关键发现：FBP剂量依赖性地抑制脂多糖（LPS）诱导的NO产生，并同时降低原代培养的鼠小胶质细胞和BV2细胞中iNOS在蛋白质和mRNA水平上的表达。 FBP显着抑制iNOS启动子活性，但稳定iNOS mRNA。在已知与iNOS表达相关的转录因子中，激活蛋白（AP-1）的激活被FBP显着阻断。 FBP抑制LPS诱导的三种MAPK亚型-p38 MAPK，JNK和ERK的磷酸化。 FBP抑制LPS诱导的活性氧（ROS）产生并降低细胞内GSSG / GSH比。意义：我们的发现表明FBP通过抑制JNK和p38 MAPK减弱LPS诱导的iNOS表达，这可能与ROS的下调有关。

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