Department of Orthopedics, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310005, P.R. China.
Department of Orthopedics Surgery, Fuyang Orthopedics and Traumatology Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 311400, P.R. China.
Mol Med Rep. 2020 Sep;22(3):2032-2042. doi: 10.3892/mmr.2020.11254. Epub 2020 Jun 18.
Osteoarthritis (OA) is a chronic disease that is mainly characterized by chondrocyte degeneration. Inflammatory mediators participate in the development of OA, leading to chondrocyte apoptosis and destruction of the cartilage. Genistein is the major active component of isoflavone, with a chemical composition and a biological effect that is similar to that of estrogens, which prevents the degradation of cartilage; however, its underlying mechanisms of action remain unknown. The aim of the present study was to investigate the anti‑apoptotic effects of genistein on chondrocytes for the treatment of inflammation‑induced OA. Interleukin (IL)‑1β was used to establish a chondrocyte OA model. After treatment with different concentrations of genistein, western blotting identified that expression levels of collagen II and aggrecan were increased in a concentration‑dependent manner, while caspase 3 expression gradually decreased after genistein application. Moreover, flow cytometry and ELISA results demonstrated that genistein could decrease chondrocyte apoptosis and reduce the levels of tumor necrosis factor (TNF)‑α in a dose‑dependent manner. Furthermore, the in vitro data were evaluated in an OA rat model. Genistein increased the collagen and acid glycosaminoglycan content, as well as decreased the levels of TNF‑α and IL‑1β. Genistein also promoted the expression levels of collagen II and aggrecan in the articular cartilage, and decreased the expression of caspase 3, thus alleviating cartilage degradation. In conclusion, the results indicated that genistein mediated inflammation and had an anti‑apoptotic role in treating OA. Therefore, genistein may serve as an alternative treatment for OA.
骨关节炎（OA）是一种主要以软骨细胞退变为特征的慢性疾病。炎症介质参与 OA 的发生发展，导致软骨细胞凋亡和软骨破坏。染料木黄酮是异黄酮的主要活性成分，其化学组成和生物学作用与雌激素相似，可防止软骨降解；然而，其作用机制尚不清楚。本研究旨在探讨染料木黄酮对软骨细胞的抗凋亡作用，用于治疗炎症诱导的 OA。白细胞介素（IL）-1β用于建立软骨细胞 OA 模型。用不同浓度的染料木黄酮处理后，Western blot 鉴定出胶原 II 和聚集蛋白聚糖的表达水平呈浓度依赖性增加，而 caspase 3 的表达在染料木黄酮应用后逐渐下降。此外，流式细胞术和 ELISA 结果表明，染料木黄酮可剂量依赖性降低软骨细胞凋亡并降低 TNF-α水平。此外，在 OA 大鼠模型中评估了体外数据。染料木黄酮增加了胶原和酸性糖胺聚糖的含量，并降低了 TNF-α和 IL-1β的水平。染料木黄酮还促进了软骨中胶原 II 和聚集蛋白聚糖的表达水平，并降低了 caspase 3 的表达，从而减轻了软骨降解。综上所述，结果表明染料木黄酮介导炎症并在治疗 OA 中具有抗凋亡作用。因此，染料木黄酮可能成为 OA 的一种替代治疗方法。
