International Journal of Molecular Sciences · 2016 · 56 citations · 21 references
DentistryPathobiologyPharmacologyApoptosisCartilage RepairInflammationCartilage BreakdownCartilage DegenerationCartilage MetabolismIntra-articular TherapyJoint DiseaseOsteoarthritisArticular Cartilage LossCartilage Degradation MechanismsCartilage DestructionIntra-articular AdministrationMatrix MetalloproteinasesOxidative Stress In CartilageOxidative Stress InjuryProteoglycan Loss
Osteoarthritis (OA) is the most prevalent joint disease. Dietary intake of vitamin C relates to a reduction in cartilage loss and OA. This study examined the efficacy of vitamin C to prevent OA with the in vitro chondrosarcoma cell line (SW1353) and the in vivo monosodium iodoacetate (MIA)-induced OA rat. Results demonstrated that, in SW1353 cells, treatment with 5 μM MIA inhibited cell growth and increased oxidative stress, apoptosis, and proteoglycan loss. In addition, the expression levels of the pro-inflammatory cytokines IL-6, IL-17A, and TNF-α and matrix metalloproteinases (MMPs) MMP-1, MMP-3, and MMP-13 were increased. All of these MIA-induced changes could be prevented with treatment of 100 μM vitamin C. In an animal model, intra-articular injection of MIA-induced cartilage degradation resembled the pathological changes of OA, and treatment of vitamin C could lessen these changes. Unexpectedly, vitamin C's effects did not strengthen with the increasing dosage, while the 100 mg/kg dosage was more efficient than the 200 or 300 mg/kg dosages. Vitamin C possessed multiple capacities for prevention of OA progress, including a decrease in apoptosis and in the expression of pro-inflammatory cytokines and MMPs in addition to the well-known antioxidation.
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Mutation of the mouse klotho gene leads to a syndrome resembling ageing.
PubMed · 1997 · 66.6K citations