Effects of Bojungchiseub-tang on the Production of Inflammatory Adipokine and MAPK Signaling in 3T3-L1 Mature Adipocytes

Soo-Jung Lee
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Abstract

Adipocytes are endocrine cells that release bioactive mediators called adipokines. In condition of obesity characterized by low-grade chronic inflammation, adipocytes release inflammatory adipokines, which is related to insulin resistance. Bojungchiseub-tang (BJCST) has been used in symptoms and signs of edema, dampness-phlegm, kidney failure, and so on in Korean medicine. BJCST is also expected to have anti-obesity activities. In the present study, we examined whether BJCST modulate the production of inflammatory adipokines and the activations of the mitogen-activated protein kinases (MAPK) signaling pathway related to induce adipocyte inflammation to elucidate the effects and its mechanism of BJCST on lowering the content of inflammatory adipokines in 3T3-L1 adipocytes. As a result, BJCST suppressed the production of proinflammatory cytokines, tumor necrosis factor (TNF) -α, interleukin (IL) -1β, IL-6, interferon (IFN) -γ, granulocyte-macrophage colony-stimulating factor (GM-CSF), monocyte chemoattractant protein-1 (MCP-1), and the production of other inflammatory mediators, prostaglandin E2(PGE2) and nitric oxide(NO)viadownregulationofcyclooxygenase-2(COX-2)andinducible NO synthase (iNOS) gene expressions. In addition, BJCST decreased the phosphorylation of MAPK that promotes the production of inflammatory adipokines in 3T3-L1 mature adipocytes. In conclusion, BJCST could regulate the production of inflammatory adipokines and MAPK signaling pathway related to induction of adipose inflammation. keywords : Bojungchiseub-tang (BJCST), obesity, 3T3-L1 adipocyte, adipokines, mitogen-activated protein kinases (MAPK) signaling
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保贞解毒汤对3T3-L1成熟脂肪细胞炎性脂肪因子及MAPK信号传导的影响
脂肪细胞是一种内分泌细胞,可以释放被称为脂肪因子的生物活性介质。在以低度慢性炎症为特征的肥胖状态下,脂肪细胞释放炎性脂肪因子,与胰岛素抵抗有关。保正祛痰汤在韩国医学上被用于治疗水肿、湿痰、肾衰竭等症状和体征。bjst也有望开展抗肥胖活动。本研究通过研究BJCST是否调节炎性脂肪因子的产生和诱导脂肪细胞炎症相关的丝裂原活化蛋白激酶(MAPK)信号通路的激活,阐明BJCST降低3T3-L1脂肪细胞炎性脂肪因子含量的作用及其机制。结果,BJCST通过下调环氧化酶-2(COX-2)和诱导NO合成酶(iNOS)基因表达,抑制促炎细胞因子、肿瘤坏死因子(TNF) -α、白细胞介素(IL) -1β、IL-6、干扰素(IFN) -γ、粒细胞-巨噬细胞集落刺激因子(GM-CSF)、单核细胞趋化蛋白-1 (MCP-1)的产生,以及其他炎症介质、前列腺素E2(PGE2)和一氧化氮(NO)的产生。此外,BJCST降低了促进3T3-L1成熟脂肪细胞中炎性脂肪因子产生的MAPK的磷酸化。综上所述,BJCST可以调节炎性脂肪因子的产生以及与脂肪炎症诱导相关的MAPK信号通路。关键词:Bojungchiseub-tang (BJCST),肥胖,3T3-L1脂肪细胞,脂肪因子,丝裂原活化蛋白激酶(MAPK)信号传导
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