author_facet Wang, Yonggang
Wu, Hao
Xin, Ying
Bai, Yang
Kong, Lili
Tan, Yi
Liu, Feng
Cai, Lu
Wang, Yonggang
Wu, Hao
Xin, Ying
Bai, Yang
Kong, Lili
Tan, Yi
Liu, Feng
Cai, Lu
author Wang, Yonggang
Wu, Hao
Xin, Ying
Bai, Yang
Kong, Lili
Tan, Yi
Liu, Feng
Cai, Lu
spellingShingle Wang, Yonggang
Wu, Hao
Xin, Ying
Bai, Yang
Kong, Lili
Tan, Yi
Liu, Feng
Cai, Lu
Oxidative Medicine and Cellular Longevity
Sulforaphane Prevents Angiotensin II-Induced Testicular Cell Death via Activation of NRF2
Cell Biology
Aging
General Medicine
Biochemistry
author_sort wang, yonggang
spelling Wang, Yonggang Wu, Hao Xin, Ying Bai, Yang Kong, Lili Tan, Yi Liu, Feng Cai, Lu 1942-0900 1942-0994 Hindawi Limited Cell Biology Aging General Medicine Biochemistry http://dx.doi.org/10.1155/2017/5374897 <jats:p>Although angiotensin II (Ang II) was reported to facilitate sperm motility and intratesticular sperm transport, recent findings shed light on the efficacy of Ang II in stimulating inflammatory events in testicular peritubular cells, effect of which may play a role in male infertility. It is still unknown whether Ang II can induce testicular apoptotic cell death, which may be a more direct action of Ang II in male infertility. Therefore, the present study aims to determine whether Ang II can induce testicular apoptotic cell death and whether this action can be prevented by sulforaphane (SFN) via activating nuclear factor (erythroid-derived 2)-like 2 (NRF2), the governor of antioxidant-redox signalling. Eight-week-old male C57BL/6J wild type (WT) and<jats:italic> Nrf2</jats:italic> gene knockout mice were treated with Ang II, in the presence or absence of SFN. In WT mice, SFN activated testicular NRF2 expression and function, along with a marked attenuation in Ang II-induced testicular oxidative stress, inflammation, endoplasmic reticulum stress, and apoptotic cell death. Deletion of the<jats:italic> Nrf2</jats:italic> gene led to a complete abolishment of these efficacies of SFN. The present study indicated that Ang II may result in testicular apoptotic cell death, which can be prevented by SFN via the activation of NRF2.</jats:p> Sulforaphane Prevents Angiotensin II-Induced Testicular Cell Death via Activation of NRF2 Oxidative Medicine and Cellular Longevity
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title Sulforaphane Prevents Angiotensin II-Induced Testicular Cell Death via Activation of NRF2
title_unstemmed Sulforaphane Prevents Angiotensin II-Induced Testicular Cell Death via Activation of NRF2
title_full Sulforaphane Prevents Angiotensin II-Induced Testicular Cell Death via Activation of NRF2
title_fullStr Sulforaphane Prevents Angiotensin II-Induced Testicular Cell Death via Activation of NRF2
title_full_unstemmed Sulforaphane Prevents Angiotensin II-Induced Testicular Cell Death via Activation of NRF2
title_short Sulforaphane Prevents Angiotensin II-Induced Testicular Cell Death via Activation of NRF2
title_sort sulforaphane prevents angiotensin ii-induced testicular cell death via activation of nrf2
topic Cell Biology
Aging
General Medicine
Biochemistry
url http://dx.doi.org/10.1155/2017/5374897
publishDate 2017
physical 1-12
description <jats:p>Although angiotensin II (Ang II) was reported to facilitate sperm motility and intratesticular sperm transport, recent findings shed light on the efficacy of Ang II in stimulating inflammatory events in testicular peritubular cells, effect of which may play a role in male infertility. It is still unknown whether Ang II can induce testicular apoptotic cell death, which may be a more direct action of Ang II in male infertility. Therefore, the present study aims to determine whether Ang II can induce testicular apoptotic cell death and whether this action can be prevented by sulforaphane (SFN) via activating nuclear factor (erythroid-derived 2)-like 2 (NRF2), the governor of antioxidant-redox signalling. Eight-week-old male C57BL/6J wild type (WT) and<jats:italic> Nrf2</jats:italic> gene knockout mice were treated with Ang II, in the presence or absence of SFN. In WT mice, SFN activated testicular NRF2 expression and function, along with a marked attenuation in Ang II-induced testicular oxidative stress, inflammation, endoplasmic reticulum stress, and apoptotic cell death. Deletion of the<jats:italic> Nrf2</jats:italic> gene led to a complete abolishment of these efficacies of SFN. The present study indicated that Ang II may result in testicular apoptotic cell death, which can be prevented by SFN via the activation of NRF2.</jats:p>
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author Wang, Yonggang, Wu, Hao, Xin, Ying, Bai, Yang, Kong, Lili, Tan, Yi, Liu, Feng, Cai, Lu
author_facet Wang, Yonggang, Wu, Hao, Xin, Ying, Bai, Yang, Kong, Lili, Tan, Yi, Liu, Feng, Cai, Lu, Wang, Yonggang, Wu, Hao, Xin, Ying, Bai, Yang, Kong, Lili, Tan, Yi, Liu, Feng, Cai, Lu
author_sort wang, yonggang
container_start_page 1
container_title Oxidative Medicine and Cellular Longevity
container_volume 2017
description <jats:p>Although angiotensin II (Ang II) was reported to facilitate sperm motility and intratesticular sperm transport, recent findings shed light on the efficacy of Ang II in stimulating inflammatory events in testicular peritubular cells, effect of which may play a role in male infertility. It is still unknown whether Ang II can induce testicular apoptotic cell death, which may be a more direct action of Ang II in male infertility. Therefore, the present study aims to determine whether Ang II can induce testicular apoptotic cell death and whether this action can be prevented by sulforaphane (SFN) via activating nuclear factor (erythroid-derived 2)-like 2 (NRF2), the governor of antioxidant-redox signalling. Eight-week-old male C57BL/6J wild type (WT) and<jats:italic> Nrf2</jats:italic> gene knockout mice were treated with Ang II, in the presence or absence of SFN. In WT mice, SFN activated testicular NRF2 expression and function, along with a marked attenuation in Ang II-induced testicular oxidative stress, inflammation, endoplasmic reticulum stress, and apoptotic cell death. Deletion of the<jats:italic> Nrf2</jats:italic> gene led to a complete abolishment of these efficacies of SFN. The present study indicated that Ang II may result in testicular apoptotic cell death, which can be prevented by SFN via the activation of NRF2.</jats:p>
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spelling Wang, Yonggang Wu, Hao Xin, Ying Bai, Yang Kong, Lili Tan, Yi Liu, Feng Cai, Lu 1942-0900 1942-0994 Hindawi Limited Cell Biology Aging General Medicine Biochemistry http://dx.doi.org/10.1155/2017/5374897 <jats:p>Although angiotensin II (Ang II) was reported to facilitate sperm motility and intratesticular sperm transport, recent findings shed light on the efficacy of Ang II in stimulating inflammatory events in testicular peritubular cells, effect of which may play a role in male infertility. It is still unknown whether Ang II can induce testicular apoptotic cell death, which may be a more direct action of Ang II in male infertility. Therefore, the present study aims to determine whether Ang II can induce testicular apoptotic cell death and whether this action can be prevented by sulforaphane (SFN) via activating nuclear factor (erythroid-derived 2)-like 2 (NRF2), the governor of antioxidant-redox signalling. Eight-week-old male C57BL/6J wild type (WT) and<jats:italic> Nrf2</jats:italic> gene knockout mice were treated with Ang II, in the presence or absence of SFN. In WT mice, SFN activated testicular NRF2 expression and function, along with a marked attenuation in Ang II-induced testicular oxidative stress, inflammation, endoplasmic reticulum stress, and apoptotic cell death. Deletion of the<jats:italic> Nrf2</jats:italic> gene led to a complete abolishment of these efficacies of SFN. The present study indicated that Ang II may result in testicular apoptotic cell death, which can be prevented by SFN via the activation of NRF2.</jats:p> Sulforaphane Prevents Angiotensin II-Induced Testicular Cell Death via Activation of NRF2 Oxidative Medicine and Cellular Longevity
spellingShingle Wang, Yonggang, Wu, Hao, Xin, Ying, Bai, Yang, Kong, Lili, Tan, Yi, Liu, Feng, Cai, Lu, Oxidative Medicine and Cellular Longevity, Sulforaphane Prevents Angiotensin II-Induced Testicular Cell Death via Activation of NRF2, Cell Biology, Aging, General Medicine, Biochemistry
title Sulforaphane Prevents Angiotensin II-Induced Testicular Cell Death via Activation of NRF2
title_full Sulforaphane Prevents Angiotensin II-Induced Testicular Cell Death via Activation of NRF2
title_fullStr Sulforaphane Prevents Angiotensin II-Induced Testicular Cell Death via Activation of NRF2
title_full_unstemmed Sulforaphane Prevents Angiotensin II-Induced Testicular Cell Death via Activation of NRF2
title_short Sulforaphane Prevents Angiotensin II-Induced Testicular Cell Death via Activation of NRF2
title_sort sulforaphane prevents angiotensin ii-induced testicular cell death via activation of nrf2
title_unstemmed Sulforaphane Prevents Angiotensin II-Induced Testicular Cell Death via Activation of NRF2
topic Cell Biology, Aging, General Medicine, Biochemistry
url http://dx.doi.org/10.1155/2017/5374897