基于"亢害承制"理论探讨巨噬细胞极化在RA免疫炎症中的作用机制OA

Rheumatoid arthritis(RA)is an autoimmune disease characterized primarily by chronic synovial inflammation and progressive joint destruction,driven by immune dysregulation.Macrophages,as key regulators of immunity,can polarize into pro-inflammatory(M1)or anti-inflammatory(M2)phenotypes,thereby playing a dual regulatory role in inflammatory responses.Drawing on the traditional Chinese medicine(TCM)theory of"harmful hyperactivity and responding inhibition"—which describes how the body maintains homeostasis through intrinsic inhibitory mechanisms under pathological excess—this review examines the relationship between this theory,macrophage polarization,and immune inflammation in RA.It further explores how TCM modulates macrophage polarization by targeting signaling pathways such as NF-κB,PI3K/Akt,and Notch.The discussion covers multiple aspects of RA pathogenesis,including inflammatory responses,oxidative stress,protease/antiprotease imbalance,autophagy,apoptosis,and metabolic abnormalities.Through these mechanisms,TCM helps restore the M1/M2 balance and suppresses excessive inflammation.Guided by the"harmful hyperactivity and responding inhibition"theory,this review proposes a therapeutic strategy for RA that focuses on regulating macrophage polarization as a key approach to controlling immune inflammation.The aim is to provide a theoretical and practical foundation for the clinical prevention and treatment of RA.