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.
An efficient and "green" catalytic conversion of 2'-hydroxychalcones to flavanones in 15 min in the presence of a simple amino acid and a base at room temperature is reported. Liquiritigenin was also efficiently synthesised under these conditions.
This work aimed to investigate the effects of p‐synephrine on the differentiation of adipocyte and explore the underlying mechanism. We found that p‐synephrine suppressed the 3T3‐L1 cell adipogenesis by reducing the expression level of CCAAT/enhancer‐binding protein α (C/EBPα) and peroxisome proliferator‐activated receptor γ (PPARγ), which subsequently led to a reduction in the fatty acid‐binding protein 4 (aP2) expression. p‐Synephrine treatment markedly activated the protein kinase B (PKB/Akt) pathway and sequentially inhibited glycogen synthase kinase 3β (GSK3β) activity. Inhibition of GSK3β activity by LiCl was found to partially ameliorate the above‐mentioned effects. All these data suggested that p‐synephrine exhibited the anti‐adipogenic effects via the regulation of Akt signaling pathway and the suppression of adipogenesis‐related proteins.
Practical applications
Citrus aurantium often uses as herbal or dietary supplement in various countries around the world, including in Seville, Spain and South Africa. In traditional Chinese herbs, it is referred to as “Fructus aurantii immaturus,” “Zhi shi,” or “Zhi ke,” and has been used for hundreds of years for various digestive problems. Its primary protoalkaloid, p‐synephrine, exhibited lipolytic effects and energy expenditure, which has rapidly replaced ephedrine as an “ephedra‐free” alternative dietary supplement. The current study firstly demonstrated the anti‐adipogenic effects of p‐synephrine in 3T3‐L1 preadipocytes, which was due to the regulation of Akt signaling pathway and the subsequent suppression of adipogenesis‐related proteins. The present study may offer invaluable opinions into the mechanisms of body weight/fat‐losing activities of p‐synephrine in theory, and scientific experimental evidence on dietary supplement in practice. p‐Synephrine could be utilized for the preventive and therapeutic uses against metabolic syndrome.
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