Osteoarthritis (OA) is a degenerative joint disease that is characterized by localized inflammatory and secondary proliferative changes. Suppressor of cytokine signaling 3 (SOCS3) is elevated during OA development. We investigated the effects of this protein on human chondrocyte survival in OA and the inflammatory response together with the mechanisms of these effects. Small interfering RNA (siRNA) was used to knock down the expression of SOCS3 in interleukin(IL)-1β-induced primary human osteoarthritic chondrocytes. We found that siRNA-mediated SOCS3 knock-down in human osteoarthritic chondrocytes increased production of IL-1β-induced prostaglandin E, cell growth, transcript level and nuclear translocation of cyclin D1. Silencing of SOCS3 resulted in altered expression of nuclear factor-kappa-B (NF-κB) and cyclooxygenase (COX2). Our findings indicate that enhanced SOCS3 could have contradictory influences on OA development. SOCS3 might protect damaged joints by its anti-inflammatory effect and by inhibition of over-augmented cartilage tissue repair, which could exhibit inhibitory properties for joint inflammation, abnormal chondrocyte clustering and osteophyte formation in OA. On the other hand, SOCS3 might reduce chondrocyte growth response, which would delay repair of subchondral cancellous bone damage in OA owing to its anti-proliferation effect. The anti-inflammation and growth inhibition effects exhibited by enhanced SOCS3 in OA appear to be related to its capacity to down-regulate expression levels of NF-κB and COX2.
Our previous study showed that Semen sojae germinatum (SSG), a soy-derived Chinese medicinal material, have potential benefits for knee osteoarthritis (OA). This study was undertaken to identify the major effective sub-fraction of SSG. The 95% ethanol extract of SSG was successively fractionated into petroleum ether, ethyl acetate, n-butanol and aqueous fractions. Then we examined the effect of fractions on the inflammatory response and cell proliferation of primary human osteoarthritic chondrocytes stimulated by interleukin (IL)-1β, a recognized and common inducer of OA in vitro. Results showed that the petroleum ether, ethyl acetate and n-butanol extracts of SSG promoted cell-proliferation measured by MTT [3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazoliumbromide] assay, increased the transcript levels and nuclear translocation of cyclin D1, and inhibited the production of pro inflammatory mediator prostaglandin (PG)E 2 and nitric oxide (NO) induced by IL-1β in human OA chondrocytes, suggesting SSG extracts possessed chondro protective and anti-inflammatory properties. The ethyl acetate fraction was superior to other fractions. These data indicated SSG extracts might become a potential treatment option for humans with OA.
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