Department of Orthopedics, Ganzhou Municipal Hospital, Ganzhou, Jiangxi 341000, China.
Department of Orthopedics, The People's Hospital of Jianyang City, Jianyang, Sichuan 641400, China.
Tissue Cell. 2022 Oct;78:101865. doi: 10.1016/j.tice.2022.101865. Epub 2022 Jul 16.
Osteoarthritis (OA) is a highly prevalent chronic joint disease that involves extracellular matrix (ECM) degradation and articular cartilage inflammation. Polydatin (PD) can alleviate inflammatory reactions in numerous diseases. The present study aimed to investigate the chondroprotective and anti-inflammatory effects of PD on interleukin (IL)- 1β-treated chondrocytes in vitro and anterior cruciate ligament transection-induced rat OA models in vivo. Primary chondrocytes were isolated from SD rats and cultured. Only second-passage cells were used for subsequent experiments. Counting kit-8, quantitative real-time polymerase chain reaction, western blotting, enzyme-linked immunosorbent assay, and immunofluorescence were used to detect relevant indices. Rat OA models were established to obtain in vivo data. PD treatment decreased the production of nitric oxide (NO), prostaglandin E2 (PGE2), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), and IL-6 during IL-1β-stimulated chondrocyte inflammation. Moreover, PD upregulated aggrecan and collagen II expression, whereas downregulated a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5) and matrix metalloproteinase-13 (MMP-13) expression on IL-1β-mediated chondrocytes. Additionally, PD reduced IL-1β-stimulated NF-κB and Wnt/β-catenin activation and nuclear translocation. The results of histological analysis and scoring revealed that OA in the rat models was effectively ameliorated by the intra-articular injection of PD. PD suppressed IL-1β-stimulated iNOS, COX-2, NO, and PGE2 production, TNF-α, IL-6, collagen X, MMP-13, and ADAMTS-5 expression, collagen II and aggrecan degeneration by inhibiting NF-κB and Wnt/β-catenin signaling in vitro. PD also mitigated OA progression in the rat models, thereby providing reliable data that PD could serve as a promising candidate for OA therapy.
骨关节炎（OA）是一种高度流行的慢性关节疾病，涉及细胞外基质（ECM）降解和关节软骨炎症。虎杖苷（PD）可以减轻许多疾病中的炎症反应。本研究旨在研究 PD 对体外白细胞介素（IL）-1β处理的软骨细胞和体内前交叉韧带横断诱导的大鼠 OA 模型的软骨保护和抗炎作用。从 SD 大鼠中分离原代软骨细胞并进行培养。只有第二代细胞用于后续实验。使用细胞计数试剂盒-8、实时定量聚合酶链反应、Western blot、酶联免疫吸附试验和免疫荧光检测相关指标。建立大鼠 OA 模型以获得体内数据。PD 治疗降低了 IL-1β刺激软骨细胞炎症时一氧化氮（NO）、前列腺素 E2（PGE2）、诱导型一氧化氮合酶（iNOS）、环氧化酶-2（COX-2）、肿瘤坏死因子-α（TNF-α）和 IL-6 的产生。此外，PD 上调了软骨聚糖和胶原 II 的表达，而下调了软骨寡聚基质蛋白 5（ADAMTS5）和基质金属蛋白酶 13（MMP-13）在 IL-1β介导的软骨细胞中的表达。此外，PD 减少了 IL-1β刺激的 NF-κB 和 Wnt/β-catenin 激活和核转位。组织学分析和评分的结果表明，关节内注射 PD 有效改善了大鼠模型中的 OA。PD 通过抑制 NF-κB 和 Wnt/β-catenin 信号通路，抑制 IL-1β刺激的 iNOS、COX-2、NO 和 PGE2 产生、TNF-α、IL-6、胶原 X、MMP-13 和 ADAMTS-5 表达、胶原 II 和软骨聚糖降解，在体外减轻 OA 进展。PD 还减轻了大鼠模型中的 OA 进展，从而提供了可靠的数据，表明 PD 可能是 OA 治疗的有前途的候选药物。
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