Liquiritigenin inhibits IL-1β-induced inflammation and cartilage matrix degradation in rat chondrocytes
Liquiritigenin inhibits IL-1β-induced inflammation and cartilage matrix degradation in rat chondrocytes
复制标题
甘草素抑制大鼠软骨细胞中 IL-1β 诱导的炎症和软骨基质降解
DOI：
10.1016/j.ejphar.2019.172445
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发表时间：
2019-09-05
影响因子：
5
通讯作者：
Wu, Hua
中科院分区：
文献类型：
--
作者：
Tu, Chang;Ma, Yongzhuang;Wu, Hua
骨关节炎（OA）是一种与年龄相关的关节病，被认为与炎症损伤和软骨退化有关。甘草素（Liquiritigenin，LG）是甘草根茎中的主要活性成分，在许多炎症性疾病中表现出良好的抗炎和抗氧化作用。然而，LG对OA的影响仍不清楚。本研究旨在探讨LG对白细胞介素-1 β（IL-β 1）诱导的大鼠软骨细胞损伤的治疗作用及其机制。结果表明，LG能抑制IL-1 β诱导的NO和PGE（2）的表达。LG还能抑制IL-1 β诱导的诱导型一氧化氮合酶（iNOS）和环氧合酶-2（COX-2）的产生，同时抑制IL-1 β诱导的软骨基质分解酶（包括聚集蛋白聚糖酶-2（ADAMTS 5）和基质金属蛋白酶（MMPs））的上调。此外，LG还能减轻IL-1 β诱导的II型胶原和聚集蛋白聚糖的降解。此外，LG还能防止IL-1 β处理的大鼠软骨外植体的软骨损伤。LG通过抑制丝裂原活化蛋白激酶（MAPK）和核因子-κ B（NF-kappa B）途径发挥作用。总之，本研究揭示了LG对IL-β处理的大鼠软骨细胞的抗炎特性及其可能的机制，这可能为OA治疗提供新的思路。
Osteoarthritis (OA) is an age-related arthropathy which has been considered to be associated with inflammatory damage and cartilage degradation. Liquiritigenin (LG), the main bioactive component of the rhizomes of Glycyrrhiza uralensis, has exhibited promising anti-inflammatory and anti-oxidative potential in numerous inflammatory diseases. However, the effects of LG on OA remain unclear. In this study, the therapeutic effects as well as the underlying mechanisms of LG on interleukin-1 beta (IL-beta 1)-treated rat chondrocytes had been investigated. Our results showed that LG could inhibit the IL-1 beta-induced expression of nitic oxide (NO) and prostaglandin E-2 (PGE(2)). In consist with these findings, the IL-1 beta-induced production of inducible nitic oxide synthase (iNOS) and cyclooxygenase-2 (COX2) could also be decreased by LG. Meanwhile, LG could suppress the IL-1 beta-induced upregulation of cartilage matrix catabolic enzymes including aggrecanase-2 (ADAMTS5) and matrix metalloproteinases (MMPs). Besides, the IL-1 beta-induced degradation of collagen II and aggrecan could be alleviated by LG. Moreover, LG prevented cartilage damage in IL-beta-treated rat cartilage explants. Mechanistically, LG functioned by inhibiting mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-kappa B) pathways activation. In general, this study reveals the anti-inflammatory properties of LG on IL-beta-treated rat chondrocytes and the possible mechanisms behind it, which may provide new ideas for OA therapy.