Xanthohumol suppresses inflammation in chondrocytes and ameliorates osteoarthritis in mice

Osteoarthritis (OA), manifested as degeneration and damage of the articular cartilage is a progressive disease of joints. Previous studies have shown that extracellular matrix degradation and inflammation have quite a significant performance in the occurrence and development of OA. In various maladies, an anti-inflammatory effect has been demonstrated for Xanthohumol (XN); while OA is an inflammation related disease. The current in vivo and in vitro study aimed to investigate the therapeutic effect of XN on OA as well as its working mechanism. The results showed that XN has the capability to hinder the expression of nitric oxide synthase (INOS), IL-1 beta-promoted inducible nitric oxide (NO), necrosis factor-alpha of tumor (TNF-alpha), interleukin-6 (IL-6), and cyclooxygenase-2 (COX-2) in vitro. In addition, XN has been found to down-regulate the expression of matrix metalloproteinase-13 and prothrombin stimulated by IL-1 beta and up-regulates type II collagen and Aggrecan expression. At the same time, it was discovered that XN activates nuclear factor (Nrf2) in chondrocytes stimulated by IL-1 beta and inhibits nuclear factor B (NF-kappa B) signal transduction. The DMM model manifests that XN has an inhibitory impact on the progression of osteoarthritis and thus may be a candidate drug to slow down and delay the development of OA.

Automated summary

The research found that Xanthohumol (XN) can inhibit the expression of nitric oxide synthase (INOS), IL-1 beta-promoted inducible nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and cyclooxygenase-2 (COX-2) in vitro. Additionally, it down-regulates matrix metalloproteinase-13 and prothrombin, while up-regulating type II collagen and Aggrecan expression. XN also activates nuclear factor (Nrf2) and inhibits nuclear factor B (NF-kappaB) signal transduction to slow down the progression of osteoarthritis.