Department of Chemistry and Biochemistry, University of Alaska Fairbanks, Fairbanks, AK 99775-6160, USA.
Institute of Arctic Biology, University of Alaska Fairbanks, Fairbanks, AK 99775-7000, USA.
Int J Mol Sci. 2019 Jun 5;20(11):2755. doi: 10.3390/ijms20112755.
Diabetes is a contributor to morbidity across the globe and is often associated with obesity, metabolic syndrome and other inflammatory diseases associated with aging. In addition to genetic and lifestyle factors, environmental factors such as metals and persistent organic pollutants may increase the severity or lower the threshold of these conditions. In cell culture, methylmercury is toxic to adipocytes and may impact adipokine secretions. In this study, we determined the effects of different concentrations of theaflavin digallate on methylmercury exposed 3T3-L1 adipocytes in cell culture. Secretions of resistin, adiponectin and lipid peroxidation product, 4-hydroxynonenal (4-HNE) were monitored using ELISA assays. Cell morphology of methylmercury and theaflavin-3,3'-digallate treated adipocytes was assessed using Lipid (Oil Red O) staining. Exposure to methylmercury increased the levels of resistin and adiponectin as well as 4-HNE when compared to the control cells. Methylmercury treated cells resulted in smaller number of adipocytes and clumped lipid droplets. These results suggest that methylmercury induces reactive oxygen species leading to development of an inflammatory response. Theaflavin-3,3'-digallate reduced the impact of methylmercury by maintaining the adipocytes morphology and secretion patterns of adiponectin, resistin and 4-hydroxynonenal. With this experimental model system other anti-inflammatory and signaling agents could be tested at the biochemical level before eventually leading to studies in animal models.
糖尿病是全球发病率的一个重要因素，通常与肥胖、代谢综合征和其他与衰老有关的炎症性疾病有关。除了遗传和生活方式因素外，环境因素如金属和持久性有机污染物可能会增加这些疾病的严重程度或降低其发病阈值。在细胞培养中，甲基汞对脂肪细胞有毒性作用，并可能影响脂肪因子的分泌。在这项研究中，我们确定了不同浓度的茶黄素-3,3′-二没食子酸酯对细胞培养中暴露于甲基汞的 3T3-L1 脂肪细胞的影响。采用 ELISA 法检测抵抗素、脂联素和脂质过氧化产物 4-羟基壬烯醛（4-HNE）的分泌。采用脂质（油红 O）染色法评估甲基汞和茶黄素-3,3′-二没食子酸酯处理的脂肪细胞的细胞形态。与对照细胞相比，暴露于甲基汞会增加抵抗素和脂联素以及 4-HNE 的水平。甲基汞处理的细胞导致脂肪细胞数量减少和脂滴聚集。这些结果表明，甲基汞诱导活性氧的产生，导致炎症反应的发生。茶黄素-3,3′-二没食子酸酯通过维持脂肪细胞形态和脂联素、抵抗素和 4-羟基壬烯醛的分泌模式，减轻了甲基汞的影响。利用这个实验模型系统，其他抗炎和信号转导剂可以在生化水平上进行测试，然后最终在动物模型中进行研究。
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