木犀草素通过TLR/MyD88/NF-κB通路参与急性痛风性关节炎大鼠的抗炎作用.

To investigate the anti-inflammatory effect of luteolin on the acute gouty arthritis (AGA) rats and the underlying mechanisms.A total of sixty rats were chosen and randomly divided into 5 groups:A control group, a monosodium urate (MSU) group, a colchicine group, 2 luteolin groups (50 mg/kg, 150 mg/kg). The AGA model of rats was established by injecting monosodium urate (MSU) at the concentration of 25 mg/mL into the ankle joint cavity. Changes of joint swelling index at different time points and the levels of interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in serum and synovial were measured. The mRNA expression of TLR2, TLR4, and MyD88 in synovial tissue was detected by real-time PCR, and the protein expression of TLR2, TLR4, MyD88, and NF-κB in synovial tissues was determined by Western blotting. The inflammatory cells of the ankle joint and its surrounding soft tissues were observed after HE staining, and the expression of NF-κB was determined by immunohistochemistry.

Compared with the MSU group, the joint swelling indexes of the luteolin group and the colchicine group were significantly decreased (P<0.05), and the levels of IL-1β, IL-6 and TNF-α were also significantly decreased (P<0.01). The mRNA levels of TLR2, TLR4, and MyD88 and the protein levels of TLR2, TLR4, MyD88, and NF-κB were significantly decreased (P<0.01).

Luteolin can reduce the inflammatory response of acute gouty arthritis via down-regulating the TLR/MyD88/NF-κB pathway, and it is expected to be an effective drug for the treatment of acute gouty arthritis.