Osteoarthritis (OA) is a common degenerative joint disease that is closely associated with inflammation. Stachydrine (STA) is a bioactive alkaloid with anti-inflammatory activity. However, the role of STA in OA remains unknown. This study aimed to explore the effects of STA on OA chondrocytes in the presence of IL-1β. Primary human OA chondrocytes were pretreated with various concentrations of STA for 2 h and then stimulated with IL-1β for 24 h. Inflammatory mediators and cytokines including NO, PGE2, TNF-α and IL-6 in chondrocytes were detected to reflect inflammation status. Production of extracellular matrix (ECM) degrading enzymes including MMP-3, MMP-13, ADAMTS-4 and ADAMTS-5 in chondrocytes was measured using ELISA. The expression levels of iNOS, COX-2, p65, p-p65, p-IκBα, and IκBα were detected by Western blot analysis. Our results showed that STA significantly suppressed IL-1β-induced inflammation with decreased levels of inflammatory mediators and cytokines including NO, PGE2, iNOS, COX-2, TNF-α and IL-6. Treatment with STA suppressed the production of ECM degrading enzymes including MMP-3, MMP-13, ADAMTS-4, and ADAMTS-5 in IL-1β-induced chondrocytes. Furthermore, STA blocked the IL-1β-mediated potentiation of NF-κB pathway in chondrocytes. In conclusion, these findings demonstrated that STA protected chondrocytes from IL-1β-induced inflammation through the NF-κB signaling pathway.

中文翻译：

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水苏碱可通过NF-κB信号通路减弱IL-1β诱导的骨关节炎软骨细胞的炎症反应。

骨关节炎（OA）是一种常见的变性关节疾病，与炎症密切相关。水苏碱（STA）是具有抗炎活性的生物活性生物碱。但是，STA在OA中的作用仍然未知。本研究旨在探讨STA在IL-1β存在下对OA软骨细胞的影响。用各种浓度的STA预处理原代人OA软骨细胞2 h，然后用IL-1β刺激24 h。检测到软骨细胞中的炎性介质和细胞因子（包括NO，PGE2，TNF-α和IL-6）反映炎症状态。使用ELISA测量软骨细胞中包括MMP-3，MMP-13，ADAMTS-4和ADAMTS-5的细胞外基质（ECM）降解酶的产生。通过蛋白质印迹分析检测iNOS，COX-2，p65，p-p65，p-IκBα和IκBα的表达水平。我们的结果表明，STA可显着抑制IL-1β诱导的炎症，同时降低炎症介质和细胞因子（包括NO，PGE2，iNOS，COX-2，TNF-α和IL-6）的水平。STA处理可抑制IL-1β诱导的软骨细胞中ECM降解酶（包括MMP-3，MMP-13，ADAMTS-4和ADAMTS-5）的产生。此外，STA阻断了软骨细胞中IL-1β介导的NF-κB途径的增强。总之，这些发现表明，STA通过NF-κB信号通路保护软骨细胞免受IL-1β诱导的炎症。IL-1β诱导的软骨细胞中的ADAMTS-5和ADAMTS-5。此外，STA阻断了软骨细胞中IL-1β介导的NF-κB途径的增强。总之，这些发现表明，STA通过NF-κB信号通路保护软骨细胞免受IL-1β诱导的炎症。IL-1β诱导的软骨细胞中的ADAMTS-5和ADAMTS-5。此外，STA阻断了软骨细胞中IL-1β介导的NF-κB途径的增强。总之，这些发现表明，STA通过NF-κB信号通路保护软骨细胞免受IL-1β诱导的炎症。