Department of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou, 320505, China.
Department of Orthopedics, The First Affiliated Hospital of Gannan Medical University, Ganzhou, 341000, China.
Future Med Chem. 2021 Sep;13(17):1451-1464. doi: 10.4155/fmc-2021-0127. Epub 2021 Jun 14.
To investigate whether kaempferol exhibited protective effects on osteoarthritis chondrocytes by modulating the XIST/miR-130a/STAT3 axis. qRT-PCR and western blot assays were used for gene and protein determination. Dual luciferase reporter and RNA immunoprecipitation assays were employed to study the interaction between miRNA and lncRNA or genes. Kaempferol decreased proinflammatory cytokine production and extracellular matrix degradation in C28/I2 cells. Additionally, kaempferol ameliorated expression and enhanced miR-130a expression. XIST interacted with miR-130a, and was identified as a target of miR-130a. Knockdown of expression suppressed proinflammatory cytokine production and extracellular matrix degradation in C28/I2 cells. Overexpression of rescued the effects of knockdown. Kaempferol inhibited inflammation and extracellular matrix degradation by modulating the XIST/miR-130a/STAT3 axis in chondrocytes.
为了研究山奈酚是否通过调节 XIST/miR-130a/STAT3 轴对骨关节炎软骨细胞发挥保护作用。采用 qRT-PCR 和 Western blot 检测基因和蛋白。双荧光素酶报告和 RNA 免疫沉淀实验用于研究 miRNA 和 lncRNA 或基因之间的相互作用。山奈酚降低 C28/I2 细胞中促炎细胞因子的产生和细胞外基质的降解。此外,山奈酚改善了 XIST 的表达,并增强了 miR-130a 的表达。XIST 与 miR-130a 相互作用,并被鉴定为 miR-130a 的靶基因。下调 XIST 的表达抑制 C28/I2 细胞中促炎细胞因子的产生和细胞外基质的降解。过表达 XIST 可挽救 XIST 敲低的作用。山奈酚通过调节软骨细胞中的 XIST/miR-130a/STAT3 轴抑制炎症和细胞外基质降解。