“天俞”配对激活Keap1/Nrf2/HO-1通路：对类风湿关节炎炎症和氧化应激的影响
Activation of the Keap1/Nrf2/HO-1 Pathway by "Tianyu" Pairing: Implications for Inflammation and Oxidative Stress in Rheumatoid Arthritis.
作者信息
Tang Lu, Li Mingquan, Piao Songlan, Du Lianyun, Qiu Saiyue, Jiang Xin, Luo Meixiu, Wang Yinghang, Pan Zhi
机构信息
Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin, China.
Third Affiliated Clinical Hospital of the Changchun University of Chinese Medicine, Changchun, Jilin, China.
出版信息
Endocr Metab Immune Disord Drug Targets. 2025;25(6):479-491. doi: 10.2174/0118715303307608240812114651.
OBJECTIVE
The objective of this study was to examine the impact of "Tianyu" Pairing on oxidative stress in the development of Rheumatoid arthritis (RA) and approach its potential mechanism using cell experiments.
METHODS
A cell model of RA was developed by stimulating rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS) with tumor necrosis factor-α (TNF-α). This model aimed to assess the impact of serum containing Rhodiola rosea-Euonymus alatus drug pair (TYP) on inflammation and oxidative stress in the development of RA, specifically through the Keap1/Nrf2/HO-1 pathway.
RESULTS
The findings from the experiment demonstrated that the presence of TYP in the serum effectively suppressed the proliferation of RA-FLS induced by TNF-α. Additionally, TYP facilitated the apoptosis of afflicted cells, attenuated the migratory and invasive capabilities of diseased cells, and decreased the levels of Kelch ECH associating protein 1 (Keap1), reactive oxygen species (ROS), glutathione peroxidase (GSH-Px), catalase (CAT), and malondialdehyde (MDA) (p < 0.01). The influence of inflammation and oxidative stress in RA-FLS cells was reduced by increasing the nuclear-cytoplasmic ratio of Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2) and levels of phosphorylated Nrf2, Heme Oxygenase 1 (HO-1), and Superoxide Dismutase (SOD) (p < 0.01).
CONCLUSION
TYP can regulate inflammation and oxidative stress in RA-FLS cells by activating the Keap1/Nrf2/HO-1 pathway.
目的
本研究旨在探讨“天榆”药对对类风湿关节炎（RA）发病过程中氧化应激的影响，并通过细胞实验探讨其潜在机制。
方法
通过用肿瘤坏死因子-α（TNF-α）刺激类风湿关节炎成纤维样滑膜细胞（RA-FLS）建立RA细胞模型。该模型旨在评估含红景天-鬼箭羽药对（TYP）的血清对RA发病过程中炎症和氧化应激的影响，具体通过Keap1/Nrf2/HO-1信号通路来实现。
结果
实验结果表明，血清中的TYP有效抑制了TNF-α诱导的RA-FLS增殖。此外，TYP促进了病变细胞的凋亡，减弱了病变细胞的迁移和侵袭能力，并降低了Kelch ECH结合蛋白1（Keap1）、活性氧（ROS）、谷胱甘肽过氧化物酶（GSH-Px）、过氧化氢酶（CAT）和丙二醛（MDA）的水平（p<0.01）。通过增加核因子红细胞2相关因子2（Nrf2）的核质比以及磷酸化Nrf2、血红素加氧酶1（HO-1）和超氧化物歧化酶（SOD）的水平，降低了RA-FLS细胞中炎症和氧化应激的影响（p<0.01）。
结论
TYP可通过激活Keap1/Nrf2/HO-1信号通路调节RA-FLS细胞中的炎症和氧化应激。
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