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PI3K/Akt/FoxO pathway mediates glycolytic metabolism in HepG2 cells exposed to triclosan (TCS).
Environment International ( IF 10.3 ) Pub Date : 2020-01-06 , DOI: 10.1016/j.envint.2019.105428 Jing An 1 , Huixin He 1 , Weiwei Yao 1 , Yu Shang 1 , Yun Jiang 2 , Zhiqiang Yu 3
Environment International ( IF 10.3 ) Pub Date : 2020-01-06 , DOI: 10.1016/j.envint.2019.105428 Jing An 1 , Huixin He 1 , Weiwei Yao 1 , Yu Shang 1 , Yun Jiang 2 , Zhiqiang Yu 3
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Triclosan (TCS) has been widely used as an antibacterial agent for the last several decades in personal care products. The toxicological effect of TCS has attracted more and more attention of researchers. The purpose of this study is to evaluate the cytotoxic effects of TCS in HepG2 cells and to elucidate the molecular mechanism focusing on regulation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/forkhead box O (FoxO) pathway in the glycolytic metabolism. In this study, we evaluated the adverse effect of TCS exposure on cell viability, reactive oxygen species (ROS) generation, superoxide dismutase (SOD) activity and mitochondrial membrane potential (MMP). In addition, the glycolysis process in HepG2 cells exposed to TCS was examined in terms of glucose consumption, lactate production and ATP generation. Furthermore, Affymetrix Human U133 plus 2.0 gene chips and gene function enrichment analysis were conducted to screen differential expression genes (DEGs) and potential signaling pathway. Expressions of the glycolysis-related proteins were measured and quantified with Western Blotting. The results showed that TCS could suppress the cell viability, induce oxidative stress, and cause mitochondrial damage. In addition, TCS exposure promoted the glycolysis process, as manifested by accelerated conversion of glucose to lactate and increased energy release. Western Blotting results confirmed that the expression levels of glycolysis related proteins were significantly elevated. The PI3K/Akt/FoxO pathway was identified to play a pivot role in TCS-induced glycolysis, which was further confirmed by inhibitor tests using specific inhibitors LY294002 and MK2206. In general, TCS can induce oxidative stress, cause oxidative damages and promote glycolysis in HepG2 cells, which was mediated by the PI3K/Akt/FoxO pathway.
中文翻译：
PI3K / Akt / FoxO途径介导暴露于三氯生（TCS）的HepG2细胞中的糖酵解代谢。
在过去的几十年中，三氯生（TCS）已广泛用作个人护理产品中的抗菌剂。TCS的毒理作用已引起越来越多的研究者的关注。这项研究的目的是评估TCS在HepG2细胞中的细胞毒性作用，并阐明侧重于调节磷脂酰肌醇3-激酶（PI3K）/蛋白激酶B（Akt）/叉头盒O（FoxO）途径的分子机制。糖酵解代谢。在这项研究中，我们评估了TCS暴露对细胞活力，活性氧（ROS）生成，超氧化物歧化酶（SOD）活性和线粒体膜电位（MMP）的不利影响。另外，从葡萄糖消耗，乳酸产生和ATP产生方面检查了暴露于TCS的HepG2细胞中的糖酵解过程。此外，进行了Affymetrix Human U133 plus 2.0基因芯片和基因功能富集分析，以筛选差异表达基因（DEG）和潜在的信号通路。测定糖酵解相关蛋白的表达，并用蛋白质印迹法定量。结果表明，TCS可以抑制细胞活力，诱导氧化应激并引起线粒体损伤。此外，TCS暴露促进了糖酵解过程，这表现为葡萄糖向乳酸的加速转化和能量释放的增加。Western Blotting结果证实糖酵解相关蛋白的表达水平显着升高。已确定PI3K / Akt / FoxO途径在TCS诱导的糖酵解中起关键作用，这一点通过使用特异性抑制剂LY294002和MK2206的抑制剂测试进一步证实。
更新日期：2020-01-07
中文翻译：
PI3K / Akt / FoxO途径介导暴露于三氯生（TCS）的HepG2细胞中的糖酵解代谢。
在过去的几十年中，三氯生（TCS）已广泛用作个人护理产品中的抗菌剂。TCS的毒理作用已引起越来越多的研究者的关注。这项研究的目的是评估TCS在HepG2细胞中的细胞毒性作用，并阐明侧重于调节磷脂酰肌醇3-激酶（PI3K）/蛋白激酶B（Akt）/叉头盒O（FoxO）途径的分子机制。糖酵解代谢。在这项研究中，我们评估了TCS暴露对细胞活力，活性氧（ROS）生成，超氧化物歧化酶（SOD）活性和线粒体膜电位（MMP）的不利影响。另外，从葡萄糖消耗，乳酸产生和ATP产生方面检查了暴露于TCS的HepG2细胞中的糖酵解过程。此外，进行了Affymetrix Human U133 plus 2.0基因芯片和基因功能富集分析，以筛选差异表达基因（DEG）和潜在的信号通路。测定糖酵解相关蛋白的表达，并用蛋白质印迹法定量。结果表明，TCS可以抑制细胞活力，诱导氧化应激并引起线粒体损伤。此外，TCS暴露促进了糖酵解过程，这表现为葡萄糖向乳酸的加速转化和能量释放的增加。Western Blotting结果证实糖酵解相关蛋白的表达水平显着升高。已确定PI3K / Akt / FoxO途径在TCS诱导的糖酵解中起关键作用，这一点通过使用特异性抑制剂LY294002和MK2206的抑制剂测试进一步证实。
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