4.3 Article

Troxerutin Reduces Kidney Damage against BDE-47-Induced Apoptosis via Inhibiting NOX2 Activity and Increasing Nrf2 Activity

Journal

OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
Volume 2017, Issue -, Pages -

Publisher

HINDAWI LTD
DOI: 10.1155/2017/6034692

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Funding

  1. National Natural Science Foundation of China [31200873, 81171012, 81271225, 81400902]
  2. Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
  3. 333 Project Award of Jiangsu Province
  4. Qinglan Project of the Young and Middle-aged Academic Leader of Jiangsu College and University
  5. Major Fundamental Research Program of the Natural Science Foundation of the Jiangsu Higher Education Institutions of China [13KJA180001]
  6. Graduate Student Innovation Program of Jiangsu Province [KYZZ16_04678]

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2,2,4,4-Tetrabromodiphenyl ether (BDE-47), one of the persistent organic pollutants, seriously influences the quality of life; however, its pathological mechanism remains unclear. Troxerutin is a flavonoid with pharmacological activity of antioxidation and anti-inflammation. In the present study, we investigated troxerutin against BDE-47-induced kidney cell apoptosis and explored the underlying mechanism. The results show that troxerutin reduced renal cell apoptosis and urinary protein secretion in BDE-47-treated mice. Western blot analysis shows that troxerutin supplement enhanced the ratio of Bcl-2/Bax; inhibited the release of cytochrome c from mitochondria, the activation of procaspase-9 and procaspase-3, and the cleavage of PARP; and reduced FAS, FASL, and caspase-8 levels induced by BDE-47. In addition, troxerutin decreased the production of reactive oxygen species (ROS) and increased the activities of antioxidative enzymes. Furthermore, troxerutin blunted Nrf2 ubiquitylation, enhanced the activity of Nrf2, decreased the activity of NOX2, and ameliorated kidney oxidant status of BDE-47-treated mice. Together, these results confirm that troxerutin could alleviate the cytotoxicity of BDE-47 through antioxidation and antiapoptosis, which suggests that its protective mechanism is involved in the inhibition of apoptosis via suppressing NOX2 activity and increasing Nrf2 signaling pathway.

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