PurposeInterleukin 6 (IL-6) and IL-8 participate in the pathogenesis of chronic rhinosinusitis with nasal polyps, and their levels are increased by prostaglandin E2 (PGE2) in different cell types. The purposes of this study were to determine whether PGE2 has any effect on the increase in the levels of IL-6 and IL-8 in nasal polyp-derived fibroblasts (NPDFs) and subsequently investigate the possible mechanism of this effect.MethodsDifferent concentrations of PGE2 were used to stimulate NPDFs at different time intervals. NPDFs were treated with agonists and antagonists of E prostanoid (EP) receptors. To determine the signaling pathway for the expression of PGE2-induced IL-6 and IL-8, PGE2 was treated with Akt and NF-κB inhibitors in NPDFs. Reverse transcription-polymerase chain reaction for IL-6 and IL-8 mRNAs was performed. IL-6 and IL-8 levels were measured byenzyme-linked immunosorbent assay (ELISA). The activation of Akt and NF-κB was evaluated by western blot analysis.ResultsPGE2 significantly increased the mRNA and protein expression levels of IL-6 and IL-8 in NPDFs. The EP2 and EP4 agonists and antagonists induced and inhibited IL-6 expression. However, the EP4 agonist and antagonist were only observed to induce and inhibit IL-8 expression level. The Akt and NF-κB inhibitors significantly blocked PGE2-induced expression of IL-6 and IL-8.ConclusionsPGE2 increases IL-6 expression via EP2 and EP4 receptors, and IL-8 expression via the EP4 receptor in NPDFs. It also activates the Akt and NF-κB signal pathways for the production of IL-6 and IL-8 in NPDFs. These results suggest that signaling pathway for IL-6 and IL-8 expression induced by PGE2 might be a useful therapeutic target for the treatment of nasal polyposis.
Red ginseng is an immune-enhancing compound that exhibits anti-inflammatory action. The ginsenoside Rg1, an ingredient of red ginseng, has been shown to play an important role in tumor suppression, wound healing, and angiogenesis. This study evaluated the effects of red ginseng extract and Rg1 in a diabetic wound model. Diabetes was induced with streptozotocin (STZ) in 8-week-old male Institute of Cancer Research (ICR) mice weighing 30–35 g. A full-thickness skin defect was treated by applying a dressing every 3 days. The mice were divided into three groups. Group 1 was administered an extract of red ginseng (10 mg/kg/d, n = 27, oral) and group 2 was administered Rg1 (10 mg/kg/d, n = 27, oral). Group 3 was a control group treated with phosphate-buffered saline (0.3 mL/kg/d, n = 27, oral). Red ginseng extract and Rg1 were orally administered to mice daily for 10 days following injury in groups 1 and 2, respectively. Both increased mRNA and protein levels of vascular endothelial growth factor (VEGF) and transforming growth factor (TGF)-β1 compared to controls. In addition, the wounds of animals in the Rg1 group were significantly smaller between days 7 and 10 (p < 0.05). VEGF and TGF-β1 were not expressed in diabetic mice in the control group. Both red ginseng extract and Rg1 promoted the production of VEGF and TGF-β1, which are important in wound healing. Our results for Rg1 suggest its potential to promote diabetic wound healing by stimulating the production or activity of VEGF and TGF-β1 factors involved in the wound healing process.
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