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首页> 外文期刊>Cytokine >Effects of 17 beta-estradiol and progesterone on the production of adipokines in differentiating 3T3-L1 adipocytes: Role of Rho-kinase
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Effects of 17 beta-estradiol and progesterone on the production of adipokines in differentiating 3T3-L1 adipocytes: Role of Rho-kinase

机译：17β-雌二醇和孕酮对分化3T3-L1脂肪细胞中脂肪因子产生的影响：Rho激酶的作用

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Effect of female sex hormones on the production/release of adipocyte-derived cytokines has been debatable. Furthermore, whether the cellular signaling triggered by these hormones involve Rho-kinase has not been investigated yet. Therefore, in this study, effects of 17 beta-estradiol and progesterone as well as the Rho-kinase inhibitor, Y-27632 on the level of adipokines such as resistin, adiponectin, leptin, TNF-alpha and IL-6 were investigated in 3T3-L1-derived adipocytes. Differentiation was induced in the post-confluent preadipocytes by the standard differentiation medium (Dulbecco's modified Eagle's medium with 10% fetal bovine serum together with the mixture of isobutylmethylxanthine, dexamethasone and insulin) in the presence of 17 beta-estradiol (10(-8)-10(-7) M), progesterone (10(-6)-10(-5) M), the Rho-kinase inhibitor, Y-27632 (10(-5) M) and their combination for 8 days. Measurements of the adipokines were performed in the culturing medium by ELISA kits using specific monoclonal antibodies. 17 beta-estradiol elevated resistin but decreased adiponectin and IL-6 levels; however, it did not alter the concentration of leptin and TNF-alpha. Y-27632 pretreatment inhibited the rise of resistin and the fall of adiponectin by 17 beta-estradiol without any effects by its own. Progesterone did not change resistin, leptin and TNF-alpha level; however, it elevated adiponectin and decreased IL-6 production. Neither 17 beta-estradiol nor Y-27632 was able to antagonize the increase of adiponectin and the reduction of IL-6 levels by progesterone. While Y-27632 alone lowered IL-6 level, it increased leptin and TNF-alpha concentration without altering resistin and adiponectin. In conclusion, 17 beta-estradiol could modify adipokine production in 3T3-L1 adipocytes with the actions some of which involve Rho-kinase mediation. (C) 2015 Elsevier Ltd. All rights reserved.
机译：女性性激素对脂肪细胞源性细胞因子产生/释放的影响尚有争议。此外，尚未研究由这些激素触发的细胞信号传导是否涉及Rho激酶。因此，在这项研究中，在3T3中研究了17种β-雌二醇和孕酮以及Rho激酶抑制剂Y-27632对诸如抵抗素，脂联素，瘦素，TNF-α和IL-6等脂肪因子水平的影响。 -L1来源的脂肪细胞。在存在17β-雌二醇（10（-8）的条件下），通过标准分化培养基（含10％胎牛血清的Dulbecco改良Eagle培养基以及异丁基甲基黄嘌呤，地塞米松和胰岛素的混合物）诱导融合后的前脂肪细胞分化。 -10（-7）M），孕酮（10（-6）-10（-5）M），Rho激酶抑制剂，Y-27632（10（-5）M）及其组合治疗8天。使用特定的单克隆抗体，通过ELISA试剂盒在培养基中进行脂肪因子的测定。 17β-雌二醇升高抵抗素但降低脂联素和IL-6水平;然而，它并没有改变瘦素和TNF-α的浓度。 Y-27632预处理通过17β-雌二醇抑制抵抗素的上升和脂联素的下降，而没有其自身的任何作用。孕酮不改变抵抗素，瘦素和TNF-α水平;然而，它增加了脂联素并降低了IL-6的产生。 17β-雌二醇和Y-27632均不能拮抗黄体酮对脂联素的增加和IL-6水平的降低。虽然单独使用Y-27632可以降低IL-6水平，但可以增加瘦素和TNF-α的浓度，而不会改变抵抗素和脂联素。总之，17β-雌二醇可以通过3种作用于Rho激酶介导的作用来改变3T3-L1脂肪细胞中脂肪因子的产生。 （C）2015 Elsevier Ltd.保留所有权利。

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