Department of Orthopaedic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, China.
Oxid Med Cell Longev. 2021 Jan 7;2021:6684147. doi: 10.1155/2021/6684147. eCollection 2021.
Intervertebral disc degeneration (IDD) and low back pain caused by IDD have attracted public attention owing to their extremely high incidence and disability rate. Oxidative stress is a major cause of IDD. Tea polyphenols (TP) are natural-derived antioxidants extracted from tea leaves. This study explored the protective role of TP on the nucleus pulposus cells (NPCs) of intervertebral discs and their underlying mechanism.
An model of HO-induced degeneration of NPCs was established. RT-qPCR and western blotting were used to detect the mRNA and protein expression of the targets. An model of IDD was established via acupuncture of the intervertebral disc. Radiological imaging and histological staining were performed to evaluate the protective role of TP.
HO contributed to NPC degeneration by inducing high levels of oxidative stress. TP treatment effectively increased the expression of nucleus pulposus matrix-associated genes and reduced the expression of degeneration factors. Further mechanistic studies showed that TP delayed HO-mediated NPC degeneration by activating the Keap1/Nrf2/ARE pathway experiments showed that TP delayed the degeneration of NPCs in rats through the Keap1/Nrf2/ARE pathway.
Our study confirmed that TP activates the Keap1/Nrf2/ARE pathway to exert an antioxidative stress role, ultimately delaying the degeneration of intervertebral discs.
椎间盘退行性变（IDD）和由 IDD 引起的下腰痛因其极高的发病率和致残率而引起了公众的关注。氧化应激是 IDD 的主要原因。茶多酚（TP）是从茶叶中提取的天然抗氧化剂。本研究探讨了 TP 对椎间盘髓核细胞（NPC）的保护作用及其潜在机制。
建立了 HO 诱导的 NPC 退变模型。使用 RT-qPCR 和 Western blot 检测靶标 mRNA 和蛋白表达。通过椎间盘针刺建立 IDD 模型。进行放射影像学和组织学染色以评估 TP 的保护作用。
HO 通过诱导高水平的氧化应激导致 NPC 退变。TP 治疗可有效增加椎间盘基质相关基因的表达，降低退变因子的表达。进一步的机制研究表明，TP 通过激活 Keap1/Nrf2/ARE 通路延迟 HO 介导的 NPC 退变。实验表明，TP 通过 Keap1/Nrf2/ARE 通路延缓了大鼠 NPC 的退变。
本研究证实，TP 通过激活 Keap1/Nrf2/ARE 通路发挥抗氧化应激作用，最终延缓椎间盘退变。
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