RESUMEN
BACKGROUND: Previous studies have found that electroacupuncture (EA) could effectively inhibit the expression of p38 and Fas mRNA mediated by MAPK signaling pathways, to further inhibit the apoptosis of chondrocytes. Meanwhile,EA delays the degeneration of articular cartilage mediated by JAK-STAT signaling pathway through upregulating the expression levels of transforming growth factor β1 as well as the mRNA expression levels of STAT3, Smad3 and LepR.OBJECTIVE: To explore the effect of EA on the cartilage ultrastructure and mRNA expression levels of Ras, Raf,MEK1/2 and ERK1/2 in the rat with knee osteoarthritis.METHODS: The rat models of knee osteoarthritis were established, and randomized into four groups at 2 weeks after modeling: model group received no interventions; 15- and 30-minute EA groups were given EA at the Hsiyen (medical,extra) of bilateral knee joints for 15 and 30 minutes, respectively; PD98059 group was given the intravenous injection of extracellular signal-regulated kinase inhibitor PD98059. The intervention time was 3 months. Those rats received normal feeding served as blank control group.RESULTS AND CONCLUSION: Transmission electron microscopy showed that compared with the model group, the chondrocytes in the 15- and 30-minute EA and PD98059 groups changed little, the nucleus was larger, partial endoplasmic reticulum cisterna expanded, and the mitochondria structure was clear. ELISA results showed that the 15-and 30-minute EA and PD98059 groups had a significant decrease in the level of tumor necrosis factor α compared with the model group (P < 0.01). RT-PCR revealed that the mRNA expression levels of Ras, Raf, MEK1/2 and ERK1/2 in the 15- and 30-minute EA and PD98059 groups were significantly downregulated (P < 0.05 or P < 0.01). These results indicate that EA can alleviate chondrocyte injury in the rat osteoarthritic model, reduce the level of tumor necrosis factor α in the synovium, and downregulated the expression levels of Ras, Raf, MEK1/2 and ERK1/2 mRNA, further delaying the chondrocyte degeneration in osteoarthritis.