Atractylodesin inhibits interleukin-1β-induced osteoarthritis of human chondrocytes

Abstract

Objective To observe the effect of atractylodesin on human osteoarthritis (OA) chondrocytes. Methods Human OA chondrocytes were pretreated with 10, 50, 100 mg/kg stractylodesin, followed by stimulation with interleukin (IL)-1β (10 μg/L) for 24 h. The expression levels of cyclooxygenase 2 (COX2) and nitric oxide (NO) were detected by enzyme linked immunosorbent assay (ELISA). The mRNA expression of matrix metalloproteinases (MMP)-1, MMP-13, COX2 and NO was measured by real-time quantitative polymerase chain reaction (Real-time PCR). Western blotting was used to examine the activity of nuclear factor-κB (NF-κB) pathway and the expression of human liver X receptor alpha (LXRα). Results Atractylodesin significantly decreased MMP-1 (618.99±12.68, 478.65±11.25, 243.17±7.88; t=5.120, P<0.05), MMP-13 (62.78±5.16, 48.35±4.28, 30.66±4.17; t=4.178, P<0.05), COX2 (71.41±4.33, 58.62±3.65, 37.48±2.52; t=4.782, P<0.05), NO (245.87±9.96, 183.26±8.47, 120.56±5.38; t=5.030, P<0.05) in human OA chondrocytes induced by IL-1β. Atractylodesin could attenuate chondrocyte inflammatory response by inhibiting IL-1β-mediated NF-κB activation. Atractylodesin can inhibit IL-1β-mediated chondrocyte inflammatory response by activating LXRα activity (P<0.05). Conclusion Atractylodesin has anti-inflammatory activity in human OA chondrocytes. Key words: Atractylodesin; Interleukin-1β; Osteoarthritis; Inflammatory response