Paeonol ameliorates monosodium urate‐induced arthritis in rats through inhibiting nuclear factor‐κB‐mediated proinflammatory cytokine production

• DOI: 10.1002/ptr.6472
• Publication Date: 2019-08-13T04:34:28Z
• Authors: Gang Chen; Ping Jia; Zhong‐yi Yin; Shu‐zhen Kong; Zhao‐bao Xiang; Xu‐xu Zheng
• Keywords: Male; 0303 health sciences; Arthritis, Gouty; Synovial Membrane; NF-kappa B; Acetophenones; Down-Regulation; Paeonia; Rats; Uric Acid; 3. Good health; Rats, Sprague-Dawley; 03 medical and health sciences; Animals; Cytokines; Inflammation Mediators; Gait Analysis; Gait; Drugs, Chinese Herbal; Signal Transduction

Moutan Cortex has been widely used to treat various types of arthritis in traditional Chinese medicine. Paeonol is isolated as an active ingredient from Moutan Cortex. However, the effect and potential mechanism of paeonol on gouty arthritis have not been evaluated. In this study, rats were treated intragastrically with paeonol for consecutive 7 days. On Day 5, rats were intra‐articularly injected with monosodium urate (MSU) crystals in the ankle joints to induce MSU‐induced arthritis (MIA). Paw volume was detected at various time points. Gait score was measured at 24 hr after MSU crystal injection. Ankle joints were collected for evaluation of histological score and expression of proinflammatory cytokines using hematoxylin and eosin staining and immunohistochemistry staining, respectively. Nuclear level of nuclear factor (NF)‐κBp65 in synovial tissues was analyzed by western blot assay. NF‐κB DNA‐binding activity was measured by enzyme linked immunosorbent assay. Paeonol markedly lowered the paw volume, gait score, and histological score in MIA rats. Mechanistically, paeonol markedly reduced the expression of TNF‐α, IL‐1β, and IL‐6 in synovial tissues of MIA rats. In addition, the elevated level of p65 in nucleus and NF‐κB DNA‐binding activity in synovial tissues of MIA rats were reduced significantly by paeonol treatment. These findings suggest that paeonol exerts anti‐inflammatory effect in MIA rats through inhibiting expression of proinflammatory cytokines and NF‐κB activation.