首页> 外文期刊>生物医学与环境科学:英文版 >Curcumin, a Potential Inhibitor of Up-regulation of TNF-alpha and IL-6 Induced by Palmitate in 3T3-L1 Adipocytes through NF-kappaB and JNK Pathway
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Curcumin, a Potential Inhibitor of Up-regulation of TNF-alpha and IL-6 Induced by Palmitate in 3T3-L1 Adipocytes through NF-kappaB and JNK Pathway

机译:姜黄素,棕榈酸酯通过NF-κB和JNK途径诱导棕榈酸酯在3T3-L1脂肪细胞中诱导TNF-α和IL-6上调的潜在抑制剂

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Objective To investigate the attenuating effect of curcumin,an anti-inflammatory compound derived from dietary spice turmeric(Curcuma longa)on the pro-inflammatory insulin-resistant state in 3T3-L1 adipocytes.Methods Glucose uptake rate was determined with the[~3H]2-deoxyglucose uptake method.Expressions of tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6) were measured by quantitative RT-PCR analysis and ELISA.Nuclear transcription factor kappaB p65 (NF-κB p65)and mitogen-activated protein kinase(MAPKs)were detected by Western blot assay.Results The basal glucose uptake was not altered,and curcumin increased the insulin-stimulated glucose uptake in 3T3-L1 ceils.Curcumin suppressed the transcription and secretion of TNF-αand IL-6 induced by palmitate in a concentration-dependent manner. Palmitate induced nuclear translocation of NF-kB.The activities of Jun NH2-terminal kinase(JNK).extracellular signal-regulated kinasel/2(ERK1/2) and p38MAPK decreased in the presence of curcumin.Moreover,pretreatment with SP600125(inhibitorof JNK)instead of PD98059 or SB203580(inhibitorofERK1/2 or p38MAPK,respectively)decreased the up-regulation of TNF-αinduced by palmitate Conclusion Curcumin reverses palmitate-induced insulin resistance state in 3T3-L1 adipocytes through the NF-kB and JNK pathway.

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