Abstract
Genistein is an isoflavone extracted from soybean (Glycine max). This compound has anti-inflammatory, anti-oxidative, and anti-cancer effects; however, the mechanism underlying the effects of genistein on IL-1β-stimulated human osteoarthritis (OA) chondrocytes remains unknown. Our objectives in this study were to explore the anti-inflammatory effects of genistein on IL-1β-stimulated human OA chondrocytes and to investigate the potential mechanisms which underlie them. Our results from an in-vitro model of osteoarthritis indicate that genistein inhibits the IL-1β-induced expression of the catabolic factors nitric oxide synthase 2 (NOS2), cyclooxygenase 2 (COX-2), and matrix metalloproteinases (MMPs). Genistein was shown to stimulate Ho-1 expression, which has been associated with Nrf-2 pathway activation in human chondrocytes. In a rat model, genistein was also shown to attenuate the progression of traumatic osteoarthritis. Taken together, these results demonstrate the effectiveness of genistein in mediating the inflammation associated with joint disorders. Our results also indicate that genistein could potentially serve as an alternative therapeutic treatment for OA.
Highlights
Osteoarthritis (OA) is the most common form of chronic arthritis
Our results revealed that genistein concentrations above 10concentrations μM/mL (i.e., 50above and diphenyltetrazolium bromide (MTT) assays
Our results revealed that genistein did not have100 a statistically significant on chondrocyte growth
Summary
Osteoarthritis (OA) is the most common form of chronic arthritis. This condition has been linked to excessive weight, injury, and genetic mutations [1,2,3]. OA involves the progressive destruction of the extracellular matrix (ECM) in articular cartilage and bone, which leads to chronic joint pain, among the elderly [4,5,6,7]. Articular cartilage degradation is caused by (1) biochemical changes related to structural and metabolic deviations and (2) an imbalance between synthesis and degradation pathways [10]. The cause of OA is not known; it is believed that the pathogenesis of this condition is related to inflammation [13]. Several inflammatory cytokines are involved in pathophysiological processes associated with OA, such as (Interleukin) IL-6, Nutrients 2019, 11, 1180; doi:10.3390/nu11051180 www.mdpi.com/journal/nutrients
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