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Exp Ther Med. 2020 Mar;19(3):1864-1870. doi: 10.3892/etm.2020.8440. Epub 2020 Jan 8.

本文引用的文献

1
Heparin inhibits the inflammation and proliferation of human rheumatoid arthritis fibroblast‑like synoviocytes through the NF‑κB pathway.肝素通过NF-κB途径抑制人类风湿性关节炎成纤维样滑膜细胞的炎症和增殖。
Mol Med Rep. 2016 Oct;14(4):3743-8. doi: 10.3892/mmr.2016.5719. Epub 2016 Sep 6.
2
Roles of NF-κB in Cancer and Inflammatory Diseases and Their Therapeutic Approaches.核因子κB在癌症和炎症性疾病中的作用及其治疗方法。
Cells. 2016 Mar 29;5(2):15. doi: 10.3390/cells5020015.
3
Cyclin G2 inhibits epithelial-to-mesenchymal transition by disrupting Wnt/β-catenin signaling.细胞周期蛋白G2通过破坏Wnt/β-连环蛋白信号传导来抑制上皮-间质转化。
Oncogene. 2016 Sep 8;35(36):4816-27. doi: 10.1038/onc.2016.15. Epub 2016 Feb 15.
4
A Dual Target-directed Agent against Interleukin-6 Receptor and Tumor Necrosis Factor α ameliorates experimental arthritis.一种针对白细胞介素-6受体和肿瘤坏死因子α的双靶点导向药物可改善实验性关节炎。
Sci Rep. 2016 Feb 4;6:20150. doi: 10.1038/srep20150.
5
A novel NF-κB/YY1/microRNA-10a regulatory circuit in fibroblast-like synoviocytes regulates inflammation in rheumatoid arthritis.成纤维样滑膜细胞中一种新型的核因子κB/阴阳1/微小RNA-10a调控环路调节类风湿关节炎中的炎症反应。
Sci Rep. 2016 Jan 29;6:20059. doi: 10.1038/srep20059.
6
Interleukin-21 induces migration and invasion of fibroblast-like synoviocytes from patients with rheumatoid arthritis.白细胞介素-21诱导类风湿关节炎患者成纤维样滑膜细胞迁移和侵袭。
Clin Exp Immunol. 2016 May;184(2):147-58. doi: 10.1111/cei.12751. Epub 2016 Feb 15.
7
Propofol promotes cell apoptosis via inhibiting HOTAIR mediated mTOR pathway in cervical cancer.丙泊酚通过抑制宫颈癌中HOTAIR介导的mTOR通路促进细胞凋亡。
Biochem Biophys Res Commun. 2015 Dec 25;468(4):561-7. doi: 10.1016/j.bbrc.2015.10.129. Epub 2015 Oct 31.
8
Propofol attenuates hydrogenperoxide-induced apoptosis in human umbilical vein endothelial cells via multiple signaling pathways.丙泊酚通过多种信号通路减轻过氧化氢诱导的人脐静脉内皮细胞凋亡。
Korean J Anesthesiol. 2015 Oct;68(5):488-95. doi: 10.4097/kjae.2015.68.5.488. Epub 2015 Sep 30.
9
Bromodomain and extra-terminal domain bromodomain inhibition prevents synovial inflammation via blocking IκB kinase-dependent NF-κB activation in rheumatoid fibroblast-like synoviocytes.溴结构域和末端外结构域溴结构域抑制通过阻断 IκB 激酶依赖性 NF-κB 激活来预防类风湿性成纤维样滑膜细胞中的滑膜炎症。
Rheumatology (Oxford). 2016 Jan;55(1):173-84. doi: 10.1093/rheumatology/kev312. Epub 2015 Aug 31.
10
Effects of Propofol and Midazolam on the Inflammation of Lungs after Intravenous Endotoxin Administration in Rats.丙泊酚和咪达唑仑对大鼠静脉注射内毒素后肺部炎症的影响。
Eurasian J Med. 2015 Jun;47(2):109-14. doi: 10.5152/eajm.2014.70.

丙泊酚通过核因子-κB通路抑制类风湿关节炎成纤维样滑膜细胞的增殖和侵袭。

Propofol inhibits cell proliferation and invasion in rheumatoid arthritis fibroblast-like synoviocytes via the nuclear factor-κB pathway.

作者信息

Wang Song, Liang Shuhong, Zhao Xiaoyu, He Yujie, Qi Yuedong

机构信息

Department of Pharmacy, The First Affiliated Hospital of Zhengzhou UniversityZhengzhou, China.

出版信息

Am J Transl Res. 2017 May 15;9(5):2429-2436. eCollection 2017.

PMID:28559993
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5446525/
Abstract

Propofol is an anesthetic drug commonly used in the clinical practice. The aim of this study is to explore the effect of propofol on the aggressive behaviors of rheumatoid arthritis fibroblast-like synoviocytes (RA-FLSs). Propofol treatment for 48 or 72 h significantly inhibited the viability of RA-FLSs, but a 24-h treatment did not produce cytotoxic effects. Propofol exposure for 48 h led to reduction of proliferation and induction of apoptosis in RA-FLSs, which was coupled with increased Bax and decreased Bcl-2 and survivin levels. Additionally, treatment with propofol for 24 h significantly suppressed the migration and invasion of RA-FLSs. Mechanistically, propofol inhibited nuclear factor-κB (NF-κB) activity. Overexpression of constitutively active NF-κB p65 reversed the inhibitory effects of propofol on RA-FLSs. Taken together, propofol exerts anti-proliferative and anti-invasive effects on RA-FLSs via the NF-κB pathway and may have therapeutic potential in treatment of RA.

摘要

丙泊酚是临床实践中常用的一种麻醉药物。本研究的目的是探讨丙泊酚对类风湿关节炎成纤维样滑膜细胞(RA-FLSs)侵袭行为的影响。丙泊酚处理48或72小时可显著抑制RA-FLSs的活力,但24小时处理未产生细胞毒性作用。丙泊酚作用48小时导致RA-FLSs增殖减少并诱导凋亡,同时Bax增加,Bcl-2和survivin水平降低。此外,丙泊酚处理24小时可显著抑制RA-FLSs的迁移和侵袭。机制上,丙泊酚抑制核因子-κB(NF-κB)活性。组成型活性NF-κB p65的过表达逆转了丙泊酚对RA-FLSs的抑制作用。综上所述,丙泊酚通过NF-κB途径对RA-FLSs发挥抗增殖和抗侵袭作用,可能在类风湿关节炎治疗中具有治疗潜力。