从分子机制到植物干预:骨衰老中炎症与氧化应激的双向调节
From molecular mechanism to plant intervention: the bidirectional regulation of inflammation and oxidative stress in bone aging.
作者信息
Li Qi, Zhao Xiumei, Wang Anning, Hang Tingting, Zhao Jianpeng, Zhang Shengkai, Zeng Lingfeng, Wang Weiguo
机构信息
Department of Orthopedics, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Shandong, Jinan, China.
Second Department of Clinical Psychology, Shandong Mental Health Center, Shandong, Jinan, China.
出版信息
Front Endocrinol (Lausanne). 2025 Jul 9;16:1634580. doi: 10.3389/fendo.2025.1634580. eCollection 2025.
This article systematically elaborates the central role of inflammatory response and oxidative stress in osteoporosis (OP) and cartilage injury, and reveals the molecular mechanism by which the two damage bone homeostasis through NF-κB, RANKL and other signaling pathways. Studies have shown that plant natural products (such as hesperidin, curcumin, Epimedin B, etc.) can improve bone metabolism imbalance and delay the process of bone aging by regulating inflammatory factors (TNF-α, IL-1β) and antioxidant pathways (Nrf2/HO-1). Osteoporosis and cartilage damage promote each other to form a vicious cycle, and the intervention of plant active ingredients can target this common pathological process. Based on the current evidence, the strategy of combining anti-inflammation, anti-oxidation and mechanical regulation may provide a new direction for the prevention and treatment of bone aging-related diseases.
本文系统阐述了炎症反应和氧化应激在骨质疏松症(OP)和软骨损伤中的核心作用,并揭示了二者通过核因子κB(NF-κB)、核因子κB受体活化因子配体(RANKL)等信号通路破坏骨稳态的分子机制。研究表明,植物天然产物(如橙皮苷、姜黄素、淫羊藿苷B等)可通过调节炎症因子(肿瘤坏死因子-α、白细胞介素-1β)和抗氧化途径(核因子E2相关因子2/血红素加氧酶-1,Nrf2/HO-1)改善骨代谢失衡,延缓骨衰老进程。骨质疏松症与软骨损伤相互促进,形成恶性循环,植物活性成分的干预可针对这一共同病理过程。基于现有证据,抗炎、抗氧化与力学调节相结合的策略可能为骨衰老相关疾病的防治提供新方向。
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本文引用的文献
J Orthop Surg Res. 2025-1-3
Front Endocrinol (Lausanne). 2024