TMF通过调控Sirt1/STAT3信号通路抑制骨关节炎软骨胞外基质降解

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TMF inhibits extracellular matrix degradation in osteoarthritis cartilage by regulating the Sirt1/STAT3 signaling pathway

Abstract：Objective：Osteoarthritis（OA） is a degenerative joint disease characterized by extracelular matrix （ECM） degradation，chondrocyteapoptosis，andchronicinflammation.CartilagedestructionandECMdegenerationcontributeto jointfunctionlossanddisability.Signal transducerandactivatortranscription3（STAT3）up-regulates theexpression MMP-13，which degrades collagen II.Our previous study found that 5，7，3′，4′ -tetramethoxyflavone（TMF）exhibited protectiveeffectsonOAchondrocytes.ThisstudyaimstoinvestigatetheprotectiveroleTMFininhibitingECM degradationbymediating theSirt1/STAT3signaling pathway.Methods：RatOAmodelswereestablishedbytheinjection monosodium iodoacetate（MIA）.Hematoxylin&eosin（HE）staining and immunohistochemistry（IHC）analysis were performed. IL- 1β stimulated C28/I2 cells were used as OA-like chondrocyte cell model.Western blotting assays were used to determine the protein expresion.Results： The expression MMP-13 wasupregulated while typeI collgen expression isdownregulated，andthephosphorylationlevelSTAT3isincreasedinratOAmodels.TMFreversesthe STAT3-mediated expression MMP-13 and type V collagen.Activation STAT3 or inhibition Sirt1 function attenuates the inhibitory efect TMFonECMdegradation.Conclusion：TMFcaninhibitECMdegradationmediated by the STAT3 signal pathway by activating Sirt1 expression in OA celland animal models.

KeyWords：Osteoarthritis；Extracellarmatrixdegradation；Chondrocytes；5，7，3'，4'-tetramethoxyflavone；Signal

transduction and activator transcription

CLCNumber：R684 Document code：A ArticleID：2097-7174（2026）01-0007 -09

DOI：10.3969/j. issn. 2097-7174. 2026.01.002

程齐来，焦林惠，吴龙火（赣南医科大学药学院，江西赣州）

摘要：目的：骨关节炎（Osteoarthritis，OA）是一种以胞外基质（Extracellar matrix，ECM）降解、软骨细胞凋亡及慢性炎症为特征的退行性关节疾病。（剩余23184字）