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Oxidative Medicine and Cellular Longevity - Volume 2017 2017, Article ID 3172692, 13 pages - https:-doi.org-10.1155-2017-3172692

Research Article

Department of Anesthesiology, The Second Hospital of Jilin University, 218 Ziqiang St., Changchun, Jilin 130041, China

Department of Cardiology, The Second Hospital of Jilin University, 218 Ziqiang St., Changchun, Jilin 130041, China

Department of Andrology, The First Hospital of Jilin University, 71 Xinmin St., Changchun, Jilin 130021, China

Department of Nephrology, The Second Hospital of Jilin University, 218 Ziqiang St., Changchun, Jilin 130041, China

Department of Acupuncture and Tuina, Changchun University of Chinese Medicine, 1035 Boshuo Rd., Changchun, Jilin 130117, China

The -973- National Basic Research Program of China, Changchun University of Chinese Medicine, 1035 Boshuo Rd., Changchun, Jilin 130117, China

Department of Urology, Second Division of The First Hospital of Jilin University, 3302 Jilin Rd., Changchun, Jilin 130031, China

Correspondence should be addressed to Jingyan Tian and Hao Wu

Received 25 January 2017; Revised 15 March 2017; Accepted 6 April 2017; Published 18 June 2017

Academic Editor: Alessandro Venditti

Copyright © 2017 Chenyu Pan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Activation of nuclear factor erythroid 2-related factor 2 NRF2 has been found to ameliorate diabetic testicular damage DTD in rodents. However, it was unclear whether NRF2 is required for these approaches in DTD. Epigallocatechin gallate EGCG is a potent activator of NRF2 and has shown beneficial effects on multiple diabetic complications. However, the effect of EGCG has not been studied in DTD. The present study aims to explore the role of NRF2 in both self and EGCG protection against DTD. Therefore, streptozotocin-induced diabetic C57BL-6 wild type WT and Nrf2 knockout KO mice were treated in the presence or absence of EGCG, for 24 weeks. The Nrf2 KO mice exhibited more significant diabetes-induced loss in testicular weight and spermatozoa count, and increase in testicular apoptotic cell death, as compared with the WT mice. EGCG activated NRF2 expression and function, preserved testicular weight and spermatozoa count, and attenuated testicular apoptotic cell death, endoplasmic reticulum stress, inflammation, and oxidative damage in the WT diabetic mice, but not the Nrf2 KO diabetic mice. The present study demonstrated for the first time that NRF2 plays a critical role in both self and EGCG protection against DTD.





Autor: Chenyu Pan, Shengzhu Zhou, Junduo Wu, Lingyun Liu, Yanyan Song, Tie Li, Lijuan Ha, Xiaona Liu, Fuchun Wang, Jingyan Tian,

Fuente: https://www.hindawi.com/



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