Abstract
Formation of advanced glycation end products (AGEs), which are associated with diabetes mellitus, contributes to prominent features of osteoarthritis, i.e., inflammation-mediated destruction of articular cartilage. Among the phytochemicals which play a role in anti-inflammatory effects, anthocyanins have also been demonstrated to have anti-diabetic properties. Purple corn is a source of three major anthocyanins: cyanidin-3-O-glucoside, pelargonidin-3-O-glucoside and peonidin-3-O-glucoside. Purple corn anthocyanins have been demonstrated to be involved in the reduction of diabetes-associated inflammation, suggesting that they may have a beneficial effect on diabetes-mediated inflammation of cartilage. This investigation of the chondroprotective effects of purple corn extract on cartilage degradation found a reduction in glycosaminoglycans released from AGEs induced cartilage explants, corresponding with diminishing of uronic acid loss of the cartilage matrix. Investigation of the molecular mechanisms in human articular chondrocytes showed the anti-inflammatory effect of purple corn anthocyanins and the metabolite, protocatechuic acid (PCA) on AGEs induced human articular chondrocytes via inactivation of the NFκb and MAPK signaling pathways. This finding suggests that purple corn anthocyanins and PCA may help ameliorate AGEs mediated inflammation and diabetes-mediated cartilage degradation.
Highlights
Osteoarthritis (OA), a degenerative joint disease, is caused by disturbance of anabolism and catabolism homeostasis of articular cartilage
The results of the analysis of anthocyanin content in this study are in agreement with previous studies which indicate that the major anthocyanins found in purple corn extract are cyanidin-3-glucoside (C3G), pelargonidin3-glucoside (Pg-3-glc) and peonidin-3-O-glucoside (P3G)[32,33,34,35]
The highest release of sulfated glycosaminoglycan (s-GAG) was on day 7 followed by the peak release of hyaluronic acid (HA) at day 28 followed by a decline
Summary
Osteoarthritis (OA), a degenerative joint disease, is caused by disturbance of anabolism and catabolism homeostasis of articular cartilage. The glycation of cartilage collagen is higher than that of skin collagen[9], affecting collagen conformation and properties such as loss of solubility and flexibility contributing to increased mechanical stress[10, 11] Another cause of AGEs induced OA is the interaction of AGEs with the receptor for advanced glycation end products (RAGEs) on chondrocyte cell membranes[12] which stimulates inflammation[13] via activation of the nuclear factor NF-κB and MAPK followed by up-regulation of pro-inflammatory c ytokines[14]. Previous studies have shown that anthocyanins attenuate inflammation in arthritis induced rat models and IL-1β induced bovine nasal explants[22] This phytochemical decreases type II collagen and proteoglycan degradation. A methylated anthocyanin decreases the expression of TNF-α, IL-1β and MMPs in OA rats via the inhibition of NF-κB25
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