β-arrestin 2 attenuates lipopolysaccharide-induced liver injury via inhibition of TLR4/NF-κB signaling pathway-mediated inflammation in mice

作者：Mengping Jiang, Chun Xu, Yunwei Guo, Qian-Jiang Luo, Li Lin, Huiling Liu, Jie Jiang, Huixin Chen, Xiuqing Wei · 发表于：World Journal of Gastroenterology · 年份：2018 · DOI：10.3748/wjg.v24.i2.216 · 被引用次数：27 · 研究领域：Receptor Mechanisms and Signaling、Cytokine Signaling Pathways and Interactions、Drug-Induced Hepatotoxicity and Protection

AIM: . METHODS: 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. RESULTS: 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. CONCLUSION: inhibition of TLR4/NF-κB signaling pathway-mediated inflammation.