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首页> 外文期刊>Journal of Huazhong University of Science and Technology >Effect of Tumor Necrosis Factor-α on Resistin Expression in 3T3-L1 Adipocytes and Its Mechanism
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Effect of Tumor Necrosis Factor-α on Resistin Expression in 3T3-L1 Adipocytes and Its Mechanism

机译:肿瘤坏死因子-α对3T3-L1脂肪细胞抵抗素表达的影响及其机制

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In order to investigate the effect of tumor necrosis factor-α (TNFα) on resistin expression in 3T3-L1 adipocytes, and further explore its mechanisms, the differentiated 3T3-L1 adipo-cytes were incubated with 0, 1, 10, 100 ng/mL TNFα respectively for 24 h, and then the expression of resistin was determined. The differentiated 3T3-L1 adipocytes were incubated with 100 ng/ mL TNFα for 3, 6, 24 h respectively, and then the expression of resistin mRNA was analyzed. 3T3-L1 adipocytes were induced to differentiate into mature adipocytes. The cells were randomly divided into 4 groups for culture. In the control group, no drugs were added. Cells of TNFα group were treated with 100 ng/mL TNFα . In Ro-31-8220 group, 5 μmol/L protein kinase C inhibitor Ro-31-8220 was added. With TNFα + Ro-31-8220 group, 100 ng/mL TNFα were added 1 h after the addition of 5 μmol/L Ro-31-8220. All adipocytes were cultured for 24 h. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting were employed to detect the expression of resistin gene. Our results showed that resistin protein and mRNA in 3T3-L1 adipocytes were inhibited by TNFα at different concentrations (P < 0. 01), and the inhibitory effect increased with the concentration (P < 0. 01). At the same concentrations, the inhibitory effect increased with time (P < 0. 01). Ro-31-8220 could inhibit its expression and the inhibitive effect remained unchanged with addition of TNFα (P > 0. 05). It was concluded that TNFα could inhibit the expression of resistin in 3T3-L1 adipocytes. The mechanism may be that the expression of resistin is partly controlled by protein kinase C signal conduction pathway.
机译:为了研究肿瘤坏死因子-α(TNFα)对3T3-L1脂肪细胞中抵抗素表达的影响,并进一步探讨其机制,将分化的3T3-L1脂肪细胞与0、1、10、100 ng /分别于TNFαmL处24 h,测定其抵抗素的表达。将分化的3T3-L1脂肪细胞分别与100 ng / mLTNFα孵育3、6、24 h,然后分析抵抗素mRNA的表达。诱导3T3-L1脂肪细胞分化为成熟的脂肪细胞。将细胞随机分为4组进行培养。在对照组中,没有添加药物。用100 ng / mLTNFα处理TNFα组细胞。在Ro-31-8220组中,添加了5μmol/ L蛋白激酶C抑制剂Ro-31-8220。对于TNFα+ Ro-31-8220组,在添加5μmol/ L Ro-31-8220 1小时后添加100 ng / mLTNFα。所有脂肪细胞培养24小时。采用逆转录聚合酶链反应(RT-PCR)和蛋白质印迹法检测抵抗素基因的表达。我们的结果表明,不同浓度的TNFα抑制3T3-L1脂肪细胞中的抵抗素蛋白和mRNA表达(P <0. 01),并且随着浓度的升高,抑制作用增强(P <0. 01)。在相同浓度下,抑制作用随时间增加(P <0. 01)。 Ro-31-8220能抑制其表达,且添加TNFα后其抑制作用保持不变(P> 0. 05)。结论:TNFα可以抑制3T3-L1脂肪细胞中抵抗素的表达。其机制可能是抵抗素的表达部分受蛋白激酶C信号传导途径控制。

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