Effect of emodin on chondrocyte viability in an in vitro model of osteoarthritis.

Emodin is an anthraquinone isolated from the Chinese herb Radix et Rhizoma Rhei and has been used to treat various diseases for centuries. The aim of the present study was to investigate the effect of emodin on the inflammatory mediators in rat chondrocytes. In the present study, chondrocytes were isolated from rats, cultured and harvested when they reached generation P3. Cells were treated with different doses of emodin (10, 20, and 30 µg/ml) followed by interleukin 1β (IL-1β, 10 ng/ml). Control cells were either untreated or treated with IL-1β alone. An enzyme-linked immunosorbent assay was used to measure levels of nitric oxide (NO) and prostaglandin E2 (PGE2). Reverse transcription-quantitative polymerase chain was performed to measure levels of matrix metallopeptidase (MMP)-3 and -13 mRNA. The expression of MMP-3, MMP-13, extracellular-signal regulatory kinase (ERK)1/2, phosphorylated ERK1/2 and β-catenin proteins were detected by western-blot analysis. The results demonstrated that treatment with emodin treatment reduced the cytotoxicity of IL-1β and inhibited the expression of NO and PGE2 in rat chondrocytes. Furthermore, emodin inhibited the expression of MMP3 and MMP13, and the phosphorylation of various proteins involved in the ERK and Wnt/β-catenin pathway. Therefore, emodin is able to promote the proliferation of chondrocytes by inhibiting the ERK and Wnt/β-catenin pathway and downregulating the expression of a series of inflammatory mediators in chondrocytes.