Objective : To explore the molecular mechanism of long non-coding RNA metastasis associated lung ad- enocarcinoma transcript 1 (MALAT1) / microRNA-15b-5p (miR-15b-5p) regulating the Wnt / β-catenin pathway in lipopolysaccharide (LPS) -induced chondrocyte injury in osteoarthritis． Methods : TDC5 cells were treated with 5 mg / L LPS to establish the osteoarthritis cell injury model，and the expression levels of MALAT1 and miR-15b-5p in the cells were detected by RT-qPCR. The MTT，flow cytometry，Alizarin red staining，and ELISA were used to as- sess the effects of MALAT1 and miR-15b-5p on LPS-induced chondrocyte injury．The dual-luciferase reporter gene assay was used to examine the regulatory relationship between MALAT1 and miR-15b-5p．Western blot assay was used to evaluate the expression of relevant proteins． Results : In LPS-induced ATDC5 cells，MALAT1 expression decreased (P＜0. 05) ．Compared to the control group，the LPS group exhibited reduced cell activity，an increased apoptosis rate，elevated levels of tumor necrosis factor-α , interleukin-6，and interleukin-1 β , a higher number of calcified nodules，increased expression levels of extracellular matrix degradation-related proteins MMP13 and AD- AMTS5，decreased expression levels of Collagen Ⅱ and Aggrecan，and increased protein expression levels of Wnt1 and β-catenin (P＜0. 05) ．Overexpression of MALAT1 could mitigate the effects of LPS on chondrocyte activity， apoptosis，inflammatory response，osteogenic differentiation，extracellular matrix degradation，and the Wnt / β-cate- nin pathway (P＜0. 05) ．Additionally，the overexpression of miR-15b-5p enhanced the impact of LPS on chondro- cytes (P＜0. 05) ． Conclusion MALAT1 is lowly expressed in LPS-induced chondrocytes，and it alleviates LPS- induced chondrocyte injury by targeting miR-15b-5p to inhibit the Wnt / β-catenin pathway．