Influence of heat-reinforcing Needling on the PPAR-γ/NF-κB signaling pathway in the synovial membrane of rats with rheumatoid arthritis.

The study seeks to examine how heat-reinforcing needling (HRN) affects the PPAR-γ/NF-κB signaling pathway in synovial membranes of rats with rheumatoid arthritis (RA). Forty-eight male Sprague-Dawley rats were randomly assigned to four groups (control, model, rosiglitazone, and HRN groups). RA was induced using bovine type II collagen and Freund's adjuvant in cold and moist conditions. The rats in the rosiglitazone group were given an intraperitoneal injection of 10 mg/kg rosiglitazone, whereas those in the acupuncture group received treatment at the Zusanli acupoint. Following the 14-day intervention, synovial tissue was stained with H&amp;E to examine pathological alterations and blood levels of TNF-α, IL-6, IL-1β, and IL-4. The expressions of PPAR-γ and NF-κB in synovial tissue were determined by Western blot analysis and real-time PCR. The model group exhibited higher fibrous tissue growth and inflammatory cell infiltration in comparison with the control group, but serum IL-4 and PPAR-γ expressions were inhibited (<i>p</i><0.01), and TNF-α, IL-6, IL-1β, and NF-κB expression levels in the serum were elevated (<i>p</i><0.01). In comparison with the model group, the HRN and rosiglitazone groups showed lower serum levels of TNF-α, IL-6, IL-1β, and NF-κB and higher levels of serum IL-4 and PPAR-γ (<i>p</i><0.05). In the RA cold syndrome model rats, HRN may reduce joint swelling and suppress inflammation of the synovial membrane, possibly via controlling the PPAR-γ/NF-κB signaling pathway. This method could provide a fresh therapeutic approach to RA symptom management.