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Glycyrrhizin, an HMGB1 inhibitor, Suppresses Interleukin-1β-Induced Inflammatory Responses in Chondrocytes from Patients with Osteoarthritis.
CARTILAGE ( IF 2.7 ) Pub Date : 2020-06-30 , DOI: 10.1177/1947603520934858
Shifeng Zhou 1 , Guodan Liu 2 , Zhenxing Si 1 , Luanfei Yu 1 , Limin Hou 1
Affiliation  

Background

High mobility group box 1 (HMGB1) is increased in osteoarthritis (OA) tissue and chondrocytes stimulated with interleukin-1β (IL-1β). Suppression of HMGB1 expression is correlated with reduced inflammatory responses induced by IL-1β. This study aimed to investigate how inhibition of HMGB1 by glycyrrhizin might affect inflammatory responses and viability of OA patient–derived chondrocytes treated with IL-1β.

Design

The amounts of HMGB1 in the cartilage tissue and synovial fluid in patients with OA were assessed by Western blot and enzyme-linked immunosorbent assay (ELISA). Chondrocytes were extracted from OA patients and maintained in culture. The impact of glycyrrhizin on IL-1β-induced cell toxicity and inflammatory mediators and cytokines, including prostaglandin E2 (PGE2), nitric oxide (NO), proinflammatory cytokines, and metalloproteases (MMPs), were assessed by ELISA, Western blot, quantitative real-time polymerase chain reaction, and the Griess reagent assay.

Results

We confirmed that HMGB1 was significantly upregulated in specimens acquired from patients with OA. HMGB1 inhibition by glycyrrhizin improved cell viability of chondrocytes treated with IL-1β. Glycyrrhizin suppressed IL-1β-induced upregulation of HMGB1 and inflammatory mediators and cytokines, including PGE2, NO, proinflammatory cytokines, and MMPs.

Conclusion

Our results indicate that glycyrrhizin may be a potential therapy for OA patients and these promising findings warrant further study for clinical application.



中文翻译:

Glycyrrhizin 是一种 HMGB1 抑制剂,可抑制骨关节炎患者软骨细胞中白介素 1β 诱导的炎症反应。

背景

在白细胞介素 1β (IL-1β) 刺激的骨关节炎 (OA) 组织和软骨细胞中,高迁移率组框 1 (HMGB1) 增加。HMGB1 表达的抑制与 IL-1β 诱导的炎症反应减少相关。本研究旨在探讨甘草甜素对 HMGB1 的抑制如何影响用 IL-1β 治疗的 OA 患者来源的软骨细胞的炎症反应和活力。

设计

通过蛋白质印迹和酶联免疫吸附试验(ELISA)评估OA患者软骨组织和滑液中HMGB1的含量。从OA患者中提取软骨细胞并保持在培养物中。甘草甜素对 IL-1β 诱导的细胞毒性和炎症介质和细胞因子的影响,包括前列腺素 E2 (PGE 2 )、一氧化氮 (NO)、促炎细胞因子和金属蛋白酶 (MMPs),通过 ELISA、蛋白质印迹、定量实时聚合酶链反应和 Griess 试剂测定。

结果

我们证实 HMGB1 在从 OA 患者获得的标本中显着上调。甘草甜素对 HMGB1 的抑制提高了用 IL-1β 处理的软骨细胞的细胞活力。Glycyrrhizin 抑制 IL-1β 诱导的 HMGB1 和炎症介质和细胞因子的上调,包括 PGE 2、NO、促炎细胞因子和 MMP。

结论

我们的研究结果表明,甘草甜素可能是 OA 患者的一种潜在疗法,这些有希望的发现值得进一步研究以用于临床应用。

更新日期:2020-06-30
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