Rheumatoid arthritis (RA) is a chronic inflammatory disease induced by TNF-α, which increases fibroblast-like synoviocytes inflammation, resulting in cartilage destruction. The current work sought to comprehend the pathophysiological importance of TNF-α stimulation on differential protein expression and their regulation by apigenin using and models of RA. The human RA synovial fibroblast cells were stimulated with or without TNF-α (10 ng/ml) and treated with 40 μM apigenin. and studies were performed to confirm the pathophysiological significance of apigenin on pro-inflammatory cytokines and on differential expression of TTR and RAGE proteins. TNF-α induced inflammatory response in synoviocytes revealed higher levels of IL-6, IL-1β, and TNF-α cytokines and upregulated differential expression of TTR and RAGE. results demonstrated that apigenin has a binding affinity towards TNF-α, indicating its potential effect in the inflammatory process. Both and results obtained by Western Blot analysis suggested that apigenin reduced the level of p65 (p = 0.005), TTR (p = 0.002), and RAGE (p = 0.020). The findings of this study suggested that TNF-α promotes the differential expression of pro-inflammatory cytokines, TTR, and RAGE via NF-kB pathways activation. Anti-inflammatory effect of apigenin impedes TNF-α mediated dysregulation or expression associated with RA pathogenesis.

中文翻译：

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类风湿性关节炎中靶向 TNF-α 诱导的 TTR 和 RAGE 表达：芹菜素介导的治疗方法

类风湿性关节炎（RA）是一种由 TNF-α 诱发的慢性炎症性疾病，TNF-α 会增加成纤维样滑膜细胞炎症，导致软骨破坏。目前的工作试图理解 TNF-α 刺激对差异蛋白表达的病理生理学重要性及其通过芹菜素使用和 RA 模型的调节。用或不用 TNF-α (10 ng/ml) 刺激人 RA 滑膜成纤维细胞，并用 40 μM 芹菜素处理。并进行了研究以证实芹菜素对促炎细胞因子以及 TTR 和 RAGE 蛋白差异表达的病理生理学意义。 TNF-α 诱导的滑膜细胞炎症反应显示 IL-6、IL-1β 和 TNF-α 细胞因子水平较高，并且 TTR 和 RAGE 的差异表达上调。结果表明芹菜素对 TNF-α 具有结合亲和力，表明其在炎症过程中的潜在作用。 Western Blot 分析获得的结果均表明芹菜素降低了 p65 (p = 0.005)、TTR (p = 0.002) 和 RAGE (p = 0.020) 的水平。本研究结果表明，TNF-α 通过 NF-kB 通路激活促进促炎细胞因子、TTR 和 RAGE 的差异表达。芹菜素的抗炎作用可阻止 TNF-α 介导的与 RA 发病机制相关的失调或表达。