Pyrroloquinoline quinone promotes chondrocyte proliferation and inhibits interleukin-1beta-induced chondrocyte apoptosis / 中国组织工程研究

ABSTRACT

BACKGROUND:Pyrroloquinoline quinone is found to accelerate Schwann cel proliferation and growth factor secretion, but there is no report addressing its role in articular cartilage and chondrocytes. OBJECTIVE: To investigate the role of pyrroloquinoline quinone in chondrocyte proliferation and interleukin-1β-induced chondrocyte apoptosis in the articular cartilage of knee joints and to verify the protective mechanism involved. METHODS: Chondrocytes were isolated from New Zealand white rabbits (1 month of age), digested under aseptic conditions, and cultured in DMEM/F12 in the presence of 10% fetal bovine serum to alow for proliferation until passage 2. Adherent chondrocytes were cultured in serum-free DMEM/F12 medium with 0, 6.25, 12.5, 25.0, 50.0 and 100.0 μmol/L pyrroloquinoline quinone, separately. Proliferation activity was determined by MTT at 48 hours of pyrroloquinoline quinone administration. Cel cycle was determined by flow cytometry at 30 hours after pyrroloquinoline quinone administration. Apoptosis was determined by flow cytometry folowing 24 hours of pyrroloquinoline quinone pretreatment and 15 hours of interleukin-1β induction. RESULTS AND CONCLUSION: Pyrroloquinoline quinone enhanced chondrocyte proliferation activity, increased percentage of S phase and G2/M phase in a dose dependent manner and reached the peak when the concentration of pyrroloquinoline quinone was 12.5-25.0 μmol/L (P< 0.05). Pyrroloquinoline quinone also inhibited interleukin-1β-induced chondrocyte apoptosis in early and late stage, and 25.0 μmol/L pyrroloquinoline quinone had the best effects (P < 0.05). These findings suggest pyrroloquinoline quinone can promote chondrocyte division and proliferation, and protect the cels from interleukin-1β-induced apoptosis.