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首页> 外文期刊>Journal of women’s health >Oxidative Stress in the Visceral Fat Is Elevated in Postmenopausal Women with Gynecologic Cancer
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Oxidative Stress in the Visceral Fat Is Elevated in Postmenopausal Women with Gynecologic Cancer

机译：内脏脂肪中的氧化胁迫在妇科癌症后期妇女升高

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Objectives: This study aimed to evaluate differences in oxidative stress of visceral fat between premenopausal and postmenopausal women and clarify the antioxidant effect of estrogen on adipocytes. Materials and Methods: Abdominal subcutaneous and omental visceral adipose tissues were obtained from 38 patients who underwent gynecological surgery. We measured the sizes of the adipocytes and evaluated the lipid peroxidation levels in the adipose tissues. We investigated whether estrogen inhibited the intracellular reactive oxygen species (ROS) production that was induced by hydrogen peroxide (H2O2) in 3T3-L1 adipocytes. Results: The visceral adipocytes were 1162.4m(2) and 1881.9m(2) in premenopausal and postmenopausal women, respectively; hence they were significantly larger in the latter (p0.05). The lipid peroxidation levels were 46.7nmoL/mg protein in premenopausal women and 99.6nmoL/mg protein in postmenopausal women; hence the lipid peroxidation levels were significantly higher in the latter (p0.05). Estradiol (E2) significantly reduced the intracellular ROS levels that were induced by H2O2 in 3T3-L1 adipocytes (p0.01). We determined that E2 significantly increased the expression of nuclear factor erythroid 2-related factor 2 (NRF2)-dependent antioxidant genes, heme oxygenase-1 (HO-1), NAD(P)H:quinone oxidoreductase 1 (NQO1), and the glutamate-cysteine ligase (GCL) modifier subunit genes, in 3T3-L1 adipocytes (p0.01). Conclusion: Oxidative stress in the visceral fat is higher in postmenopausal women. The expression of the antioxidant genes HO-1, NQO1, and GCL was upregulated by estrogen in 3T3-L1 adipocytes. Hence, estrogen may act as an antioxidant in the adipose tissues of premenopausal women.
机译：目的：本研究旨在评估前肢和绝经后妇女内脏脂肪脂肪脂肪氧化应激的差异，并阐明雌激素对脂肪细胞的抗氧化作用。材料和方法：从38名接受妇科手术的患者获得腹部皮下和题内阴粘物脂肪组织。我们测量了脂肪细胞的尺寸，并评估了脂肪组织中的脂质过氧化水平。我们研究了雌激素是否抑制了通过过氧化氢（H2O2）在3T3-L1脂肪细胞中诱导的细胞内反应性氧物质（ROS）产生。结果：内部肌肉和绝经后妇女的内脏脂肪细胞分别为1162.4m（2）和1881.9m（2）;因此，后者它们显着较大（P <0.05）。脂质过氧化水平在绝经后妇女妇女和99.6nmol / mg蛋白中为46.7nmol / mg蛋白;因此，后者脂质过氧化水平显着高（P <0.05）。雌二醇（E2）显着降低了H 2 O 2在3T3-L1脂肪细胞中诱导的细胞内ROS水平（P <0.01）。我们确定E2显着增加了核因子红外抗氧化抗氧化基因的核因子红斑2相关因子2（NRF2），血红素氧基酶-1（HO-1），NAD（P）H：醌氧化还原酶1（NQO1），以及谷氨酸半胱氨酸连接酶（GCL）改性剂亚基基因，3T3-L1 adipocytes（P <0.01）。结论：绝经后妇女的内脏脂肪中氧化应激更高。抗氧化基因HO-1，NQO1和GCl的表达通过雌激素在3T3-L1脂肪细胞中上调。因此，雌激素可以作为脂肪组织的抗氧化剂在绝经女性的脂肪组织中。

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