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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.

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。

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