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Paeoniflorin Antagonizes TNF-α-Induced L929 Fibroblastoma Cells Apoptosis by Inhibiting NF-κBp65 Activation

机译:eon药苷通过抑制NF-κBp65活化来拮抗TNF-α诱导的L929成纤维细胞瘤细胞凋亡

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摘要

Paeoniflorin (PF) is one of the main pharmacodynamic components of Paeonia suffruticosa Andr, which has a significant anti-inflammatory effect on rheumatoid arthritis (RA), with a mechanism related to the tumor necrosis factor α (TNF-α). The aim of the present study was to investigate the role of PF in the apoptosis and expression of NF-κBp65 of L929 fibroblastoma cells induced by TNF-α. Our results showed that different concentrations of PF can significantly reduce the growth inhibition of L929 cells. Moreover, morphological observations, Hoechst 33342 staining, and flow cytometry detection of apoptosis showed that PF can significantly attenuate the TNF-α-induced apoptosis in a dose-dependent manner. Western blot analysis revealed that TNF-α induced the activation of NF-κBp65, whereas PF treatment had a marked dose-dependent suppression on it, which indicates that its action might be associated with inhibiting NF-κB signaling pathway. These results show that PF exerts a beneficial effect on L929 cells to prevent TNF-α-induced apoptosis and expression of NF-κBp65, which would be helpful to clarify its role in the treatment of RA.
机译:eon药苷(PF)是of药Paeonia suffruticosa Andr的主要药效成分之一,对类风湿关节炎(RA)具有显着的消炎作用,其机制与肿瘤坏死因子α(TNF-α)有关。本研究的目的是研究PF在TNF-α诱导的L929成纤维细胞瘤细胞凋亡和NF-κBp65表达中的作用。我们的结果表明,不同浓度的PF可以显着降低L929细胞的生长抑制。此外,形态学观察,Hoechst 33342染色和流式细胞术检测细胞凋亡表明,PF可以剂量依赖性方式显着减弱TNF-α诱导的细胞凋亡。蛋白质印迹分析表明,TNF-α诱导了NF-κBp65的活化,而PF处理对其具有明显的剂量依赖性抑制作用,这表明其作用可能与抑制NF-κB信号通路有关。这些结果表明PF对L929细胞具有预防TNF-α诱导的凋亡和NF-κBp65表达的有益作用,这有助于阐明其在RA治疗中的作用。

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