OA是中老年人最常见骨关节病,研究表明，LncRNA-UFC1/miR-34a/MMP-13轴在OA软骨退变的发病中起着重要作用。它与软骨细胞外基质的破坏关系密切，可作为治疗OA的新靶点。前期研究表明，益气养血方对OA有较好的疗效，能抑制Lnc RNA-UFC1/miR-34a/MMP-13轴中MMP-13的分泌，促进蛋白聚糖表达；能调控Bcl-2/Bax平衡，抑制IL-1β、TNF-α释放，上调COL-II表达；促进软骨细胞增殖，有防治关节软骨退变的作用。本研究在此基础上，提出益气养血方可能介导该轴抑制软骨细胞外基质破坏、干预软骨细胞凋亡而发挥抗OA软骨退变的科学假说。以改良Hulth法制备KOA大鼠模型、体外培养的大鼠及OA患者退变软骨细胞为研究对象，采用组织病理学、分子生物学等方法，探讨益气养血方对该轴的调控作用，揭示该方抗OA软骨退变的分子机制，为其治疗OA提供理论依据。

Osteoarthritis (OA) is the most common degenerative osteoarthropathy in the middle-aged and the elderly. Recent studies have shown that LncRNA-UFC1/miR-34a/MMP-13 axis plays an important role in the occurrence and development of OA cartilage degeneration, and the close relationship between the axis and the apoptosis of chondrocytes and the destruction of extracellular matrix has led the axis as a new target for the treatment of OA. Previous studies have shown that Yiqi Yangxue Recipe has a good effect on OA patient, which could inhibit the secretion of MMP-13 in Lnc RNA-UFC1/miR-34a/MMP-13 axis, and promotes the expression of Aggrecan; It regulates the balance of Bcl-2/Bax, inhibits the release of IL-1β and TNF-α, up-regulates the expression of COL-II, promotes the proliferation and differentiation of chondrocytes, and prevents the degeneration of articular cartilage.On these grounds, we suggest that Yiqi Yangxue Decoction may play a role in anti-OA cartilage degeneration by inhibiting the destruction of extracellular matrix by regulating the LncRNA-UFC1/miR-34a/ MMP-13 axis and in chondrocyte proliferation and apoptosis. Thus, in this study, we plan to use different methods like histopathology, cytology, molecular biology and other methods in three models to explore the regulating effect of Yiqi Yangxue Decoction on LncRNA-UFC1/miR-34a/MMP-13 axis, and to reveal the molecular mechanism of its resistance to OA cartilage degeneration, and to provide the theoretical basis for the treatment of OA. The three models are as follows: the KOA rat model by modified Hulth method, and in vitro cultured rat model, and the degenerative chondrocytes model from OA patients.