Background: Osteoarthritis (OA), the most common form of arthritic disease, results from destruction of joint\ncartilage and underlying bone. It affects animals, including Asian elephants (Elephas maximus) in captivity, leading\nto joint pain and lameness. However, publications regarding OA pathogenesis in this animal are still limited.\nTherefore, this study aimed to investigate the effect of proinflammatory cytokines, including interleukin-1 beta (IL-\n1Beta), IL-17A, tumor necrosis factor-alpha (TNF-Alpha), and oncostatin M (OSM), known mediators of OA pathogenesis,\nand lipopolysaccharides on the expression of cartilaginous degrading enzymes, matrix metalloproteinase (MMP)-3\nand MMP-13, in elephant articular chondrocytes (ELACs) cultures. Anti-arthritic drugs and the active compounds of\nherbal plants were tested for their potential attenuation against overproduction of these enzymes.\nResults: Among the used cytokines, OSM showed the highest activation of MMP3 and MMP13 expression,\nespecially when combined with IL-1Beta. The combination of IL-1Beta and OSM was found to activate phosphorylation of\nthe mitogen-activated protein kinase (MAPK) pathway in ELACs. Lipopolysaccharides or cytokine-induced\nexpressions were suppressed by pharmacologic agents used to treat OA, including dexamethasone, indomethacin,\netoricoxib, and diacerein, and by three natural compounds, sesamin, andrographolide, and vanillylacetone.\nConclusions: Our results revealed the cellular mechanisms underlying OA in elephant chondrocytes, which is\ntriggered by proinflammatory cytokines or lipopolysaccharides and suppressed by common pharmacological or\nnatural medications used to treat human OA. These results provide a more basic understanding of the\npathogenesis of elephant OA, which could be useful for adequate medical treatment of OA in this animal.
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