〔Abstract〕 Objective To establish an interleukin-1β(Il-1β) induced inflammatory model of rat articular chondrocytes(ACs), and to investigate the relationship between the expression of lysine acetyltransferase 7(KAT7) under inflammatory stimulation and the senescence of ACs. Methods Primary ACs were obtained by digestion of rat knee cartilage with collagenase type Ⅱ and identified. The inflammatory model of ACs was induced by IL-1β. KAT7 was over-expressed or knocked down in ACs by adeno-associated virus infection or small interfering RNA transfection, respectively. A negative control group was set up. Transwell assay was used to detect cell migration ability. Senescent cells were stained with senescence-associated β-galactosidase(SA-β-Gal). Western blot(WB) was used to detect the protein expression levels of KAT7, collagen type II(Col Ⅱ), matrix metalloproteinase 13(MMP13), tumor protein p53(p53) and cyclin-dependent kinase inhibitor 1A(p21). The cells of negative control group and KAT7 over-expression group were performed for RNA sequencing, and WB was used to verify the related signaling pathways obtained by Kyoto encyclopedia of genes and genomes(KEGG) enrichment analysis. Results Compared with the control group, the SA-β-Gal staining was enhanced, the protein expression of Col Ⅱ decreased, the protein expression of MMP13 and p53 increased, the cell migration ability decreased, and the expression of KAT7 also increased in the ACs of rats after IL-1β stimulation. Compared with the negative control group, the SA-β-Gal staining was enhanced, the protein expression of Col Ⅱ decreased, the protein expression of MMP13, p53 and p21 increased, and the cell migration ability decreased in the KAT7 over-expression group. Compared with the negative control group, the SA-β-Gal staining was weakened, the protein expression of Col Ⅱ increased, the protein expression of MMP13, p53 and p21 decreased, and the cell migration ability was enhanced in the KAT7 knockdown inflammatory model of ACs. KEGG enrichment analysis showed that phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway was activated. Compared with the negative control group, the relative protein expression levels of phosphorylated protein kinase B(p-AKT)/AKT and phosphorylated mammalian target of rapamycin(p-mTOR)/mTOR in KAT7 over-expression group increased. The relative protein expression levels of p-AKT/AKT and p-mTOR/mTOR in KAT7 knockdown cells decreased.Conclusion Rat ACs with high expression of KAT7 exhibit senescence and osteoarthritis phenotype, and the mechanism may be related to the activation of PI3K/AKT/mTOR signaling pathway by KAT7.