Electroacupuncture ameliorates cartilage damage in a rat model of knee osteoarthritis and regulates expression of miRNAs and the TLR4/NF-κB pathway.

Background: Electroacupuncture (EA) has been shown to be effective in the treatment of knee osteoarthritis (KOA); however, its underlying mechanism remains unclear.

Methods: 40 KOA model rats were divided into control, untreated model, EA-treated model and celecoxib-treated model groups (n=10 each). Articular cartilage of the knee joint was stained with hematoxylin and eosin (HE), periodic acid-Schiff (PAS) and Alcian blue (AB)-PAS, and Moran/Mankin scores were used to evaluate articular cartilage injury across groups. Moreover, toll-like receptor (TLR)4/nuclear factor (NF)-κB pathway (TN-P)-related protein levels in the articular cartilage were detected using Western blotting. Oxidative stress and inflammatory biomarkers in the synovial fluid were measured by enzyme-linked immunosorbent assay (ELISA). MicroRNA (miRNA/miR) expression was measured by quantitative real-time polymerase chain reaction (qRT-PCR).

Results: Compared with the control group, Moran scores increased and Mankin scores decreased in the KOA model rats. In addition, compared with those in the control group, levels of superoxide dismutase (SOD), glutathione peroxidase (GSHPx) and interleukin (IL)-10 were significantly decreased, while levels of IL-1β, IL-6, tumor necrosis factor (TNF)-α, malondialdehyde (MDA) and nitric oxide (NO) were significantly increased, in the synovial fluid of the KOA model group. Protein levels of TLR4, anti-myeloid differentiation primary response protein 88 (MyD88) and p65 NF-κB phosphorylation were significantly increased in the articular cartilage of the KOA model group. EA and celecoxib treatment reversed the trends of these protein levels. Moreover, expression of miR-15a/127/140/146a/216a-5p and miR-27a-3p in the articular cartilage were markedly increased in KOA rats, while EA and celecoxib treatment reduced their expression.

Conclusions: EA reduces inflammation, oxidative stress and cartilage damage in KOA model rats, likely through regulation of the miRNA/TLR4/NF-κB pathway.