β-arrestin 2 attenuates lipopolysaccharide-induced liver injury via inhibition of TLR4/NF-κB signaling pathway-mediated inflammation in mice.
β-arrestin 2 attenuates lipopolysaccharide-induced liver injury via inhibition of TLR4/NF-κB signaling pathway-mediated inflammation in mice.
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β-arrestin 2通过抑制TLR4/NF-κB信号通路介导的炎症反应减轻内毒素诱导的小鼠肝损伤。
DOI：
10.3748/wjg.v24.i2.216
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发表时间：
2018-01-14
影响因子：
4.3
通讯作者：
Wei XQ
中科院分区：
文献类型：
--
作者：
Jiang MP;Xu C;Guo YW;Luo QJ;Li L;Liu HL;Jiang J;Chen HX;Wei XQ
研究β-arrestin 2在脂多糖（LPS）诱导的肝损伤中的作用及其可能机制。将雄性β-arrestin 2+/+和β-arrestin 2-/-C57 BL/6 J小鼠用于体内实验，并且将小鼠巨噬细胞系RAW 264.7用于体外实验。通过腹腔注射LPS或生理氯化钠溶液建立动物模型。收集血液样品和肝组织以分析肝损伤和促炎细胞因子水平。收集培养的细胞提取物以分析促炎细胞因子的产生和参与TLR 4/NF-κB信号通路的关键分子的表达。与野生型小鼠相比，β-arrestin 2基因敲除小鼠表现出更严重的LPS诱导的肝损伤和显著更高水平的促炎细胞因子，包括白细胞介素（IL）-1β、IL-6、肿瘤坏死因子（TNF）-α和IL-10。与对照组相比，β-arrestin 2 siRNA组RAW 264. 7细胞在LPS作用后6 h产生的促炎细胞因子（IL-1β、IL-6、TNF-α和IL-10）显著增加。此外，参与TLR 4/NF-κB信号通路的关键分子，包括磷酸化I κBα和磷酸化p65，上调。β-arrestin 2通过抑制TLR 4/NF-κB信号通路介导的炎症反应，对LPS诱导的肝组织损伤具有保护作用。
To study the role and the possible mechanism of β-arrestin 2 in lipopolysaccharide (LPS)-induced liver injury in vivo and in vitro. Male β-arrestin 2+/+ and β-arrestin 2-/- C57BL/6J mice were used for in vivo experiments, and the mouse macrophage cell line RAW264.7 was used for in vitro experiments. The animal model was established via intraperitoneal injection of LPS or physiological sodium chloride solution. Blood samples and liver tissues were collected to analyze liver injury and levels of pro-inflammatory cytokines. Cultured cell extracts were collected to analyze the production of pro-inflammatory cytokines and expression of key molecules involved in the TLR4/NF-κB signaling pathway. Compared with wild-type mice, the β-arrestin 2 knockout mice displayed more severe LPS-induced liver injury and significantly higher levels of pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and IL-10. Compared with the control group, pro-inflammatory cytokines (including IL-1β, IL-6, TNF-α, and IL-10) produced by RAW264.7 cells in the β-arrestin 2 siRNA group were significantly increased at 6 h after treatment with LPS. Further, key molecules involved in the TLR4/NF-κB signaling pathway, including phospho-IκBα and phosho-p65, were upregulated. β-arrestin 2 can protect liver tissue from LPS-induced injury via inhibition of TLR4/NF-κB signaling pathway-mediated inflammation.
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影响因子：
20.1
作者：
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通讯作者：
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作者：
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通讯作者：
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