Research Papers:

Protective effects of sulforaphane on di-n-butylphthalate-induced testicular oxidative stress injury in male mice offsprings via activating Nrf2/ARE pathway

Zhiqiang Qin, Jingyuan Tang, Peng Han, Xuping Jiang, Chengdi Yang, Ran Li, Min Tang, Baixin Shen, Wei Wang, Chao Qin and Wei Zhang _

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Oncotarget. 2017; 8:82956-82967. https://doi.org/10.18632/oncotarget.19981

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Zhiqiang Qin1,*, Jingyuan Tang1,*, Peng Han1,*, Xuping Jiang2, Chengdi Yang1, Ran Li1, Min Tang1, Baixin Shen3, Wei Wang1, Chao Qin1 and Wei Zhang1

1Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210009, China

2Department of Urology, Yixing People’s Hospital, Yixing 214200, China

3Department of Urology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing 210000, China

*These authors have contributed equally to this work

Correspondence to:

Wei Zhang, email: [email protected]

Keywords: sulforaphane, di-n-butylphthalate, oxidative stress injury, testis, Nrf2

Received: February 28, 2017    Accepted: July 16, 2017    Published: August 7, 2017


Di-N-butylphthalate (DBP) is one of the most common endocrine-disrupting chemicals which can disrupt human endocrine system, especially in the male reproductive system. Here, this study was aimed to determine whether sulforaphane (SFN) could protect against testicular oxidative stress injury induced by DBP in male mice offsprings. Wild-type (Nrf2+/+) and Nrf2-deficient (Nrf2-/-) timed-pregnant mice were given DBP orally from embryonic day (E)14.5 to E19.5. Subsequently, the oxidative stress markers were evaluated. Besides, Nrf2, NF-κB, I-kB, HO-1 and NQO-1 expression levels in the testis were measured by immunohistochemical staining or western blot analysis. DBP significantly reduced anogenital distance (AGD) and influenced testes growth in male mice offsprings, while SFN ameliorated these phenotypes. After DBP stimulation, the testicular morphology, testicular cell apoptosis index and the oxidative stress markers exhibited statistical differences compared with Control group, while SFN supplementation showed obvious improvements. In addition, administration of SFN could obviously increase the expression level of Nrf2 and its downstream ARE gene battery, such as HO-1, NQO-1 in the testis. Meanwhile, SFN pretreatment did not confer protection against DBP-induced testicular oxidative stress injury in Nrf2 knockout mice. Therefore, the present findings suggested that SFN could effectively protect against DBP-induced testicular oxidative stress injury through Nrf2/ARE signaling pathways in male mice offsprings.

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