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《生物医学与环境科学：英文版》
>Triclosan-induced Oxidative Stress Injury and Apoptosis by Regulating the PI3K/Akt/Caspase-3 Signaling Pathway in Human Renal Glomerular Endothelial Cells
Triclosan-induced Oxidative Stress Injury and Apoptosis by Regulating the PI3K/Akt/Caspase-3 Signaling Pathway in Human Renal Glomerular Endothelial Cells
Triclosan(TCS)is widely used in personal-care products because of its bactericidal and antibacterial properties.However,TCS and its toxic byproducts have been detected in aquatic environments,animals,and plants worldwide.TCS is a common phenolic environmental endocrine disruptor,and TCS in the environment enters the body mainly through diet and water.Most of the absorbed TCS is metabolized by the human kidneys and is eliminated in the urine[1].Some epidemiological studies have suggested a positive correlation between the TCS exposure level in urine and albumin(a biomarker of renal function),which could cause renal dysfunction[2].However,the potential effects of TCS on the mammalian kidney and its mechanisms are currently unknown.Consequently,we initiated an in vitro trial to study the molecular mechanism of cytotoxicity of TCS to glomeruli.
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机译：Eicosapentaenoic acid induces neovasculogenesis in human endothelial progenitor cells by modulating c-kit protein and pI3-K/akt/eNOs signaling pathways
