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首页> 外文期刊>Drug Design, Development and Therapy >Morusin Ameliorates IL-1β-Induced Chondrocyte Inflammation and Osteoarthritis via NF-κB Signal Pathway
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Morusin Ameliorates IL-1β-Induced Chondrocyte Inflammation and Osteoarthritis via NF-κB Signal Pathway

机译:Morusin通过NF-κB信号途径改善IL-1β诱导的软骨细胞炎症和骨关节炎

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Purpose: Osteoarthritis (OA) is one of the most common degenerative joint diseases in the world, characterized primarily by the progressive degradation of articular cartilage. Accumulating evidence has shown that Morusin, a flavonoid derived from the root bark of Morus alba (mulberry) plants, exerts unique protective properties in several diseases. However, its effects on OA, specifically, have not yet been characterized. Methods: In this study, we evaluated the anti-inflammatory effect of Morusin on mouse chondrocytes and its underlying mechanism in vitro. In addition, the protective effect of Morusin on destabilization of the medial meniscus (DMM) model was also explored in vivo. Results: In vitro, IL-1β-induced activation of inflammatory factors (TNF-α, IL-6, INOS and COX2) was dramatically suppressed by Morusin. Further, Morusin treatment inhibited the expression of ADAMTS5 and metalloproteinase (MMPs), both of which regulate extracellular matrix degradation. Morusin also decreased IL-1β-induced p65 phosphorylation and IκBα degradation. In vivo, degradation of the articular cartilage following surgical DMM, which mimicked OA pathology, was abrogated following treatment with Morusin, thus demonstrating a protective effect in the DMM model. Conclusion: Herein, we demonstrate that Morusin reduces the OA inflammatory response in vitro and protects against articular cartilage degradation in vivo potentially via regulation of the NF-κB pathway. Hence, Morusin may prove to be an effective candidate for novel OA therapeutic strategies.
机译:目的:骨关节炎(OA)是世界上最常见的退行性关节疾病之一,主要是通过关节软骨的逐渐降解。积累证据表明,Morusin,一种来自Morus alba(桑树)植物的根吠虫的黄酮类化合物,在几种疾病中发挥着独特的保护性能。然而,它对OA的影响尚未表征。方法:在本研究中,我们评估了Morusin对小鼠软骨细胞的抗炎作用及其体外潜在机制。此外,在体内还探讨了Morusin对内侧半月板(DMM)模型的稳定化的保护作用。结果:Morusin显着抑制了体外,IL-1β诱导的炎症因子激活(TNF-α,IL-6,INOS和COX2)。此外,Morusin治疗抑制了Adamts5和金属蛋白酶(MMP)的表达,两者都调节细胞外基质降解。 Morusin还降低了IL-1β诱导的P65磷酸化和IκBα降解。在体内,在用Morusin治疗后,在莫敏治疗后,患有oA病理学后的手术DMM后的关节软骨的降解,从而证明了DMM模型中的保护作用。结论:本文,我们证明Morusin在体外减少了OA炎症反应,并通过调节NF-κB途径来防止特性软骨降解。因此,Morusin可能被证明是新型OA治疗策略的有效候选人。

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