Objective To investigate the protective effect of erianin, a natural extract from Dendrobium, against interleukin-1β (IL-1β)-induced chondrocyte injury and its mechanism.

Methods An IL-1β (10 ng/mL)-induced chondrocyte injury model was established to simulate osteoarthritis. The cells were divided into six groups: the control group, cultured in normal medium, and erianin concentration gradient treatment groups (5, 10, 20, 40, and 80 nmol/L). Western blotting was used to detect the expression levels of the inflammatory proteins inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Enzyme-linked immunosorbent assay (ELISA) was used to measure the secretion levels of IL-6, tumor necrosis factor-α (TNF-α), prostaglandin E2 (PGE2), and nitric oxide (NO) in the cell supernatant. Real-time quantitative PCR (qRT-PCR) was used to analyze the mRNA expression of extracellular matrix metabolism-related genes, including Aggrecan, CollagenⅡ, matrix metalloproteinase 13 (MMP13), and a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5). Senescence-associated β-galactosidase (SA-β-gal) staining was used to observe chondrocyte senescence. Immunofluorescence was used to detect the nuclear translocation of nuclear factor-κB (NF-κB) signaling and to analyze the effect of erianin on the NF-κB pathway.

Results Within the concentration range of 0-40 nmol/L, erianin showed no obvious toxicity to chondrocytes, and there was no statistically significant difference in chondrocyte viability compared with the control group (all P ＞ 0.05). Therefore, 40 nmol/L was selected as the non-toxic concentration. Compared with the control group, IL-1β increased the expression of iNOS and COX-2 in chondrocytes (both P ＜ 0.01), and elevated the levels of PGE2, NO, IL-6, and TNF-α in the supernatant (all P ＜ 0.01). Treatment with 40 nmol/L erianin reversed the expression of the above inflammatory indicators (all P ＜ 0.01). In addition, erianin upregulated the mRNA expression of the extracellular matrix-related genes Aggrecan and CollageⅡ, downregulated the mRNA levels of ADAMTS5 and MMP13, and reduced the proportion of senescent chondrocytes (all P ＜ 0.01). Compared with the IL-1β group, the intensity of NF-κB signaling in the nucleus was significantly weakened after erianin treatment (P ＜ 0.01).

Conclusions Erianin effectively alleviates IL-1β-induced inflammatory responses in chondrocytes, reduces extracellular matrix degradation, and attenuates chondrocyte senescence by inhibiting the NF-κB signaling pathway.