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Byakangelicin 可抑制体外白细胞介素-1β诱导的小鼠软骨细胞炎症,并改善体内小鼠骨关节炎。

Byakangelicin inhibits IL-1β-induced mouse chondrocyte inflammation in vitro and ameliorates murine osteoarthritis in vivo.

机构信息

Department of Orthopedics, Shaoxing Hospital, Zhejiang University School of Medicine, Shaoxing, Zhejiang 312000, China.

Guangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Guangxi 530021, China.

出版信息

Int Immunopharmacol. 2020 Aug;85:106605. doi: 10.1016/j.intimp.2020.106605. Epub 2020 May 30.

DOI:10.1016/j.intimp.2020.106605
PMID:32485353
Abstract

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.

摘要

骨关节炎(OA)是一种慢性肌肉骨骼退行性疾病,可导致慢性疼痛和功能障碍等严重后果。由于病理复杂,目前有针对 OA 的预防性临床治疗方法。一些研究报告了当归根提取物中一种成分虎杖苷(BYA)具有潜在的抗炎作用;然而,BYA 在 OA 中的作用尚不清楚。在这项研究中,我们研究了 BYA 在体外白细胞介素(IL)-1β诱导的小鼠软骨细胞中和体内内侧半月板(DMM)小鼠 OA 模型中手术不稳定中的保护作用。在体外,BYA 治疗抑制了 IL-1β介导的诱导型一氧化氮合酶、环氧化酶-2、肿瘤坏死因子-α和 IL-6 的表达。此外,BYA 促进了 II 型胶原和聚集蛋白聚糖的表达,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,导致细胞外基质降解。此外,BYA 在 IL-1β诱导的软骨细胞中从机制上抑制了核因子-kappa B 信号通路。在 DMM 模型中也观察到 BYA 对 OA 发展的保护作用。总之,我们的结果强调了 BYA 作为 OA 治疗和预防的候选药物。

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