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Received Apr 17, 2017; Accepted Jun 18, 2017
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1. Introduction
Polybrominated diphenyl ethers (PBDEs), a kind of persistent organic pollutants (POPs), have been emerging in tremendous danger on the global environment and human health. How to prevent and treat the damage of PBDEs has become a close attention. To find specific effective techniques and drugs against PBDEs in treatment, to a large extent, depends on the molecular mechanism underlying the effect of PBDEs on tissue damage. Among 209 homologues, 2,2,4,4-tetra-brominated diphenyl ether (BDE-47) is widely distributed in biological materials with high contents. Seriously, accumulation of BDE-47 in the body causes the severe damage of tissues including the liver, kidney, and adipose tissue [1–11]. For example, the homeostasis of parathyroid hormone is disturbed by BDE-47 via decreasing the concentration of triiodothyronine (T3) and tetraiodothyronine (T4) in the blood serum of human or mouse [11]. Furthermore, the neurotoxicity of BDE-47 leads to a disordered behavior because of the decrease of synaptic protein in the central nervous system of mice [5–7, 9]. Recent findings show that BDE-47 induces apoptosis of human embryonic kidney cells, resulting in metabolic dysfunction [12]. However, the toxicological effects and underlying mechanism of kidney damage induced by BDE-47 in vivo are unclear.
Further studies show that natural products