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首页> 外文期刊>Archives of Oral Biology >1 /MT 2 melatonergic receptor agonist with serotonin 5-HT 2C receptor antagonistic properties, suppresses Prevotella intermedia lipopolysaccharide-induced production of proinflammatory mediators in murine macrophages
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1 /MT 2 melatonergic receptor agonist with serotonin 5-HT 2C receptor antagonistic properties, suppresses Prevotella intermedia lipopolysaccharide-induced production of proinflammatory mediators in murine macrophages

机译：1 / MT 2褪黑素能受体激动剂具有血清素5-HT 2C受体拮抗特性，抑制PREVOTALLA介质脂多糖诱导的鼠巨噬细胞的促炎介质的产生

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Highlights ? Agomelatine inhibits P . intermedia LPS-induced NO, IL-1β and IL-6 in RAW264.7 cells. ? LPS-induced nuclear translocation and DNA binding of p50 is blocked by agomelatine. ? P . intermedia LPS-elicited activation of STAT1and STAT3 is reduced by agomelatine. ? Agomelatine enhances mRNA level of SOCS1 in P . intermedia LPS-activated cells. ? Agomelatine may be useful in the host modulation of inflammatory periodontal disease. Abstract Objective This study was performed in an attempt to examine the influence of agomelatine in mitigating the generation of proinflammatory mediators in RAW264.7 murine macrophages exposed to lipopolysaccharide (LPS) obtained from Prevotella intermedia , a gram-negative anaerobic bacterium that is related with various types of periodontal diseases, and the molecular mechanisms behind its effects. Design LPS from P. intermedia strain ATCC 25611 was prepared employing the conventional phenol-water procedure. Conditioned culture media were analyzed for the levels of nitric oxide (NO), interleukin-1β (IL-1β) and IL-6. Real-time PCR analysis was carried out to determine the mRNA levels of inducible NO synthase (iNOS), IL-1β, IL-6 and SOCS1. Protein expression levels were evaluated by immunoblot test. NF-κB-dependent SEAP reporter assay was performed using a reporter cell line. DNA-binding activities of NF-κB subunits were analyzed utilizing the ELISA-based kits. Results Agomelatine was found to down-regulate significantly the generation of iNOS-derived NO, IL-1β and IL-6 as well as the expression of their mRNAs in cells activated with P . intermedia LPS. Agomelatine decreased NF-κB-dependent SEAP release caused by P. intermedia LPS. Agomelatine did not inhibit NF-κB transcription induced by LPS at the level of IκB-α degradation. Instead, LPS-induced nuclear translocation and DNA binding of NF-κB p50 subunit was blocked by agomelatine. P . intermedia LPS-elicited activation of STAT1 and STAT3 was reduced notably by co-treatment with agomelatine. Agomelatine showed a tendency to enhance mRNA level of SOCS1 in LPS-activated cells as well. Conclusions Agomelatine merits further evaluation to reveal its usefulness on the host modulation of periodontal disease.
机译：强调 ？胍兰抑制p。介质LPS诱导的NO，IL-1β和IL-6在RAW264.7细胞中。还LPS诱导的P50核易位和DNA结合被聚焦素封闭。还p。宫内节育器LPS引发的STAT1和STAT3的激活由阿莫米兰还减少。还胍甲岛增强了p中的SOCS1的mRNA水平。介质LPS-活性细胞。还聚茂物素可用于炎症牙周病的宿主调节。摘要目的本研究进行了试图检测胍啉在减轻暴露于Phivotella介质的脂多糖（LPS）的Raw264.7鼠巨噬细胞中的促炎介质的产生的影响。牙周病的类型，以及其效果背后的分子机制。使用常规酚醛水法制备来自P.中介质菌株ATCC 25611的LPS。分析了条件培养基，针对一氧化氮（NO），白细胞介素-1β（IL-1β）和IL-6的水平分析。进行实时PCR分析以确定诱导型没有合酶（InOS），IL-1β，IL-6和SOCS1的mRNA水平。通过免疫印迹试验评估蛋白质表达水平。使用报告细胞系进行NF-κB依赖的SHOP报告器测定。利用ELISA的试剂盒分析NF-κB亚基的DNA结合活性。结果发现莫昔洛汀显着下调InOS衍生的NO，IL-1β和IL-6的产生以及它们在用p的细胞中的MRNA的表达。介质LPS。 Agomelatine因P.介质LPS引起的NF-κB依赖性Seap释放。 Agomelatine未抑制LPS在IκB-α降解水平下诱导的NF-κB转录。相反，通过聚焦胶质蛋白阻断NF-κBP50亚基的LPS诱导的核转位和DNA结合。 p。通过用胍兰合并治疗，介质LPS引发的STAT1和STAT3的活化可显着降低。 Agomelatine表现出增强LPS活化细胞中SOCS1的mRNA水平的趋势。结论Agomelatine的进一步评估揭示其对腹期疾病的宿主调节的有用性。

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