TNF-α相关炎症机制在绝经后骨质疏松症中的作用及中药活性成分、单味药、复方干预的研究进展OA

Postmenopausal osteoporosis(PMOP)is the most common metabolic bone disease in middle-aged and elderly women,and its occurrence and progression are closely associated with inflammatory immune abnormalities induced by estrogen deficiency.With the development of osteoimmunology,tumor necrosis factor-α(TNF-α)has been recognized as an important proinflammatory cytokine linking immune activation to bone remodeling imbalance.Estrogen deficiency promotes aberrant activation of TNF-α through multilayered immune regulatory mechanisms and further enhances osteo-clast differentiation and bone resorption while suppressing osteoblast function through signaling pathways such as nuclear factor kappa B(NF-κB),Mitogen-activated protein kinase(MAPK),and phosphatidylinositol 3-kinase/protein kinase B(PI3K/Akt),ultimately leading to bone remodeling imbalance.Meanwhile,TNF-α inhibitors have been shown to im-prove bone metabolic markers and increase bone mineral density in patients with inflammatory diseases;however,their long-term safety,economic burden,and benefits on fracture outcomes remain limited.Existing studies have shown that re-ductions in inflammatory factors such as TNF-α during traditional Chinese medicine(TCM)interventions for PMOP are often accompanied by improvements in bone metabolism,suggesting that TNF-α may be one of the important associated factors in the therapeutic effects of TCM.This review summarizes the role of TNF-α in the pathogenesis of PMOP and outlines the characteristics of TNF-α changes and the related signaling pathways during TCM interventions,with the aim of providing a theoretical reference for further elucidating the therapeutic mechanisms of TCM.