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Byakangelicin inhibits IL-1β-induced mouse chondrocyte inflammation in vitro and ameliorates murine osteoarthritis in vivo.
International Immunopharmacology ( IF 4.8 ) Pub Date : 2020-05-30 , DOI: 10.1016/j.intimp.2020.106605
Tan Zhang 1 , Lei He 1 , Wanlei Yang 1 , Yanben Wang 1 , Jiaxuan Peng 2 , Peng Sun 3 , Qichang Yang 3 , Yewei Jia 1 , Kanxian Zhao 3 , Yu Qian 1
Affiliation  

Osteoarthritis (OA) is a chronic musculoskeletal degeneration disease, resulting in severe consequences such as chronic pain and functional disability. Owing to the complex pathology, there are currently available preventative clinical therapies for OA. Several studies have reported the potential anti-inflammatory effects of byakangelicin (BYA), a component of the Angelica dahurica root extract; however, the effects of BYA in OA remain unknown. In this study, we investigated the protective effects of BYA in interleukin (IL)-1β–induced mouse chondrocytes in vitro and on surgical destabilization in a medial meniscus (DMM) mouse OA model in vivo. In vitro, BYA treatment inhibited IL-1β–mediated inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor-alpha, and IL-6 expression. Moreover, BYA promoted the expression of type two collagen and aggrecan but inhibited the expression of thrombospondin motifs 5 and matrix metalloproteinases, leading to degradation of the extracellular matrix. In addition, BYA mechanistically suppressed nuclear factor-kappa B signaling in the IL-1β–induced chondrocytes. The protective effects of BYA in OA development were also observed in vivo using the DMM model. In conclusion, our results highlight BYA as a candidate for OA treatment and prevention.



中文翻译:

Byakangelicelicin在体外可抑制IL-1β诱导的小鼠软骨细胞发炎,并在体内改善鼠类骨关节炎。

骨关节炎(OA)是一种慢性肌肉骨骼变性疾病,会导致严重后果,例如慢性疼痛和功能障碍。由于病理复杂,目前有针对OA的预防性临床疗法。几项研究报告了当归根提取物中的一种成分——Bakangelicelic(BYA)的潜在抗炎作用。但是,BYA在OA中的作用仍然未知。在这项研究中,我们研究了BYA对白介素(IL)-1β诱导的小鼠软骨细胞的体外保护作用,以及对内侧半月板(DMM)小鼠OA模型体内手术失稳的保护作用。体外,BYA处理可抑制IL-1β介导的一氧化氮合酶,环氧合酶-2,肿瘤坏死因子-α和IL-6的表达。此外,BYA促进了2型胶原蛋白和蛋白聚糖的表达,但抑制了血小板反应蛋白基序5和基质金属蛋白酶的表达,从而导致细胞外基质的降解。此外,BYA机械性地抑制了IL-1β诱导的软骨细胞中的核因子-κB信号传导。使用DMM模型,还可以在体内观察到BYA对OA发育的保护作用。总之,我们的结果突出了BYA作为OA治疗和预防的候选人。

更新日期:2020-05-30
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