OBJECTIVE: Abnormal lipid metabolism plays a role that cannot be ignored in articular cartilage bone marrow lesions, synovial inflammation, and the destruction of chondrocytes (CHs). Ceramide is one of the key constructions of membrane lipid bilayers, which is an intracellular lipid mediator regulating varieties of cellular behaviors. The purpose of this study was to explore the role of ceramide and its inhibitor in the development of the CHs degeneration. PATIENTS AND METHODS: CHs were isolated from the cartilage collecting from the osteoarthritis (OA) patients, and oleic acid/palmitic (O/P) acid was used to induce CHs lipid disordered. Then, myriocin was used to inhibit the accumulation of ceramide. After that, the apoptosis, cell viability, glucose uptake, oxidative stress, and the chondrogenic gene expression were tested to evaluate the degenerated degree of CHs. RESULTS: Results revealed that O/P induced CH apoptosis, ceramide accumulation, a higher level of oxidative stress, IL-1β and MMP-13, but it also decreased the collagen-Ⅱ and SOX-9 expressions and affected the glucose uptake of CHs. After the stimulation of myriocin, the side effects induced by O/P was partly reversed. CONCLUSIONS: O/P induces the accumulation of ceramide and the degeneration of CHs, and myriocin can reject the harmful effect caused by O/P via the suppression of ceramide.
OBJECTIVE:Abnormal lipid metabolism plays a role that cannot be ignored in articular cartilage bone marrow lesions, synovial inflammation, and the destruction of chondrocytes (CHs). Ceramide is one of the key constructions of membrane lipid bilayers, which is an intracellular lipid mediator regulating varieties of cellular behaviors. The purpose of this study was to explore the role of ceramide and its inhibitor in the development of the CHs degeneration. PATIENTS AND METHODS: CHs were isolated from the cartilage collecting from the osteoarthritis (OA) patients, and oleic acid/palmitic (O/P) acid was used to induce CHs lipid disordered. Then, myriocin was used to inhibit the accumulation of ceramide. After that, the apoptosis, cell viability, glucose uptake, oxidative stress, and the chondrogenic gene expression were tested to evaluate the degenerated degree of CHs. RESULTS: Results revealed that O/P induced CH apoptosis, ceramide accumulation, a higher level of oxidative stress, IL-1β and MMP-13, but it also decreased the collagen-Ⅱ and SOX-9 expressions and affected the glucose uptake of CHs. After the stimulation of myriocin, the side effects induced by O/P was partly reversed. CONCLUSIONS: O/P induces the accumulation of ceramide and the degeneration of CHs, and myriocin can reject the harmful effect caused by O/P via the suppression of ceramide.