Vitamin C Protects Chondrocytes against Monosodium Iodoacetate-Induced Osteoarthritis by Multiple Pathways

Abstract

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.

Zinc Protects Articular Chondrocytes through Changes in Nrf2-Mediated Antioxidants, Cytokines and Matrix Metalloproteinases

“…The results of the present study showed that exposure of 5 μM MIA to SW1353 cells can increase oxidative stress, leading to cell cytotoxicity as previously described [ 23 ]. MIA exposure also intensively decreases GPx1 and Mn-SOD expression but increased GSH levels and HO-1 expression.…”

“…The results of a previous study indicated that MIA toxicity in chondrocytes reflects MIA-induced oxidative stress [ 23 ]. Herein, we examined oxidative stress by evaluating ROS production in SW1353 cells treated with 5 μM MIA in the presence or absence of 25 μM zinc for 24 h. As shown in Figure 2 , MIA induced ROS production, while zinc addition would decrease ROS production.…”

“…The histopathology of the rat left joints, stained with safranin O and fast green (Sigma-Aldrich, St. Louis, MO, USA), was analyzed as previously described [ 23 ]. The histological score of knee joints was assessed by the OARSI cartilage degeneration score [ 24 ].…”

Could Oxidative Stress Regulate the Expression of MicroRNA-146a and MicroRNA-34a in Human Osteoarthritic Chondrocyte Cultures?

“…Various agents, such as taurine and ascorbic acid, have been used as potent anti-oxidant substances with highly effective properties attenuating free radical toxicity [ 13 , 14 ]. Data from in vitro studies reported that their antioxidant property could ameliorate ROS-induced cartilage damage [ 15 , 16 , 17 ]. Taurine (2-aminoethane sulfonic acid) is a necessary amino acid involved in cartilage physiopathology and shows chondroprotective properties principally determining the increase in deposition of extracellular matrix components and in chondrocyte proliferation [ 18 ].…”

Evaluation of the effect of vitamin C on caspase 9 and oxidative stress in rheumatoid arthritis patients

“…Many studies proved a significant effect of vitamin C on apoptosis. Chiu et al (2017) examined the efficacy of vitamin C to prevent monosodium iodoacetate (MIA)induced osteoarthritis in rat. In an animal model, intraarticular injection of MIA increased oxidative stress and apoptosis which resulted in cartilage degradation.…”