Tenuigenin Prevents IL-1β-induced Inflammation in Human Osteoarthritis Chondrocytes by Suppressing PI3K/AKT/NF-κB Signaling Pathway

• DOI: 10.1007/s10753-016-0309-3
• Publication Date: 2016-02-05T05:42:25Z
• Authors: Chunlei Wang; Lihong Zeng; Tao Zhang; Jiakun Liu; Wenbo Wang
• Keywords: Inflammation; 0303 health sciences; MAP Kinase Signaling System; Interleukin-1beta; Anti-Inflammatory Agents; JNK Mitogen-Activated Protein Kinases; Nitric Oxide; Dinoprostone; 3. Good health; Phosphatidylinositol 3-Kinases; 03 medical and health sciences; Chondrocytes; Matrix Metalloproteinase 13; Osteoarthritis; Humans; Matrix Metalloproteinase 3; Matrix Metalloproteinase 1; Phosphorylation; Arthroplasty, Replacement, Knee; Extracellular Signal-Regulated MAP Kinases; Proto-Oncogene Proteins c-akt; Cells, Cultured; Drugs, Chinese Herbal

Tenuigenin (TEN), the main active component of Polygala tenuifolia, has been reported to have anti-inflammatory effects. However, the effects of TEN on IL-1β-stimulated osteoarthritis chondrocytes have not been reported. The purpose of this study was to investigate the anti-inflammatory effects and mechanism of TEN on IL-1β-stimulated human osteoarthritis chondrocytes. Human osteoarthritis chondrocytes were pretreated with or without TEN for 1 h and then stimulated with IL-1β. The production of NO and PGE2 were detected by the Griess reagent and ELISA. The expression of NF-κB and MAPKs (p38, JNK, ERK) were measured by Western blot analysis. The production of MMP-1, MMP3, and MMP13 were measured by ELISA. The results showed that treatment of TEN significantly inhibited IL-1β-induced NO and PGE2 production. TEN also suppressed IL-1β-induced MMP-1, MMP3, and MMP13 expression. Furthermore, TEN was found to inhibit IL-1β-induced NF-κB activation, PI3K, and AKT phosphorylation. In conclusion, these results suggest that TEN inhibits IL-1β-induced inflammation in human osteoarthritis chondrocytes by inhibiting PI3K/AKT/NF-κB signaling pathway.