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大鼠脂多糖诱导的炎症和骨质流失过程中细胞因子信号传导抑制因子1的表达

Suppressor of cytokine signaling 1 expression during LPS-induced inflammation and bone loss in rats.

作者信息

Souza João Antonio Chaves de, Nogueira Andressa Vilas Boas, Souza Pedro Paulo Chaves de, Oliveira Guilherme José Pimentel Lopes de, Medeiros Marcell Costa de, Garlet Gustavo Pompermaier, Cirelli Joni Augusto, Rossa Carlos

机构信息

Universidade Federal de Goiás - UFG, Faculty of Dentistry, Department of Periodontology, Goiânia, GO, Brazil.

Universidade Estadual Paulista - UNESP, School of Dentistry at Araraquara, Department of Diagnosis and Surgery, Araraquara, SP, Brazil.

出版信息

Braz Oral Res. 2017 Sep 28;31:e75. doi: 10.1590/1807-3107BOR-2017.vol31.0075.

Abstract

This study aimed to characterize the dynamics of suppressor of cytokine signaling (SOCS1) expression in a rat model of lipopolysaccharide-induced periodontitis. Wistar rats in the experimental groups were injected three times/week with LPS from Escherichia coli on the palatal aspect of the first molars, and control animals were injected with vehicle (phosphate-buffered saline). Animals were sacrificed 7, 15, and 30 days after the first injection to analyze inflammation (stereometric analysis), bone loss (macroscopic analysis), gene expression (qRT-PCR), and protein expression/activation (Western blotting). The severity of inflammation and bone loss associated with LPS-induced periodontitis increased from day 7 to day 15, and it was sustained through day 30. Significant (p < 0.05) increases in SOCS1, RANKL, OPG, and IFN-γ gene expression were observed in the experimental group versus the control group at day 15. SOCS1 protein expression and STAT1 and NF-κB activation were increased throughout the 30-day experimental period. Gingival tissues affected by experimental periodontitis express SOCS1, indicating that this protein may potentially downregulate signaling events involved in inflammatory reactions and bone loss and thus may play a relevant role in the development and progression of periodontal disease.

摘要

本研究旨在表征脂多糖诱导的大鼠牙周炎模型中细胞因子信号转导抑制因子1(SOCS1)表达的动态变化。实验组的Wistar大鼠每周3次在第一磨牙的腭侧注射来自大肠杆菌的脂多糖,对照动物注射赋形剂(磷酸盐缓冲盐水)。在首次注射后7天、15天和30天处死动物,以分析炎症(体视学分析)、骨质流失(宏观分析)、基因表达(qRT-PCR)和蛋白质表达/激活(蛋白质印迹法)。与脂多糖诱导的牙周炎相关的炎症和骨质流失的严重程度从第7天到第15天增加,并持续到第30天。在第15天,实验组与对照组相比,SOCS1、RANKL、OPG和IFN-γ基因表达显著(p<0.05)增加。在整个30天的实验期内,SOCS1蛋白表达以及STAT1和NF-κB激活均增加。受实验性牙周炎影响的牙龈组织表达SOCS1,表明该蛋白可能潜在地下调参与炎症反应和骨质流失的信号事件,因此可能在牙周疾病的发生和发展中发挥相关作用。

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