Testosterone improves erectile function through inhibition of reactive oxygen species generation in castrated rats
Testosterone is overwhelmingly important in regulating erectile physiology. However, the associated molecular mechanisms are poorly understood. The purpose of this study was to explore the effects and mechanisms of testosterone in erectile dysfunction (ED) in castrated rats. Forty male Sprague-Dawle...
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PeerJ Inc.
2016-05-01
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| Online Access: | https://peerj.com/articles/2000.pdf |
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| author | Rui Li Xianghu Meng Yan Zhang Tao Wang Jun Yang Yonghua Niu Kai Cui Shaogang Wang Jihong Liu Ke Rao |
| author_facet | Rui Li Xianghu Meng Yan Zhang Tao Wang Jun Yang Yonghua Niu Kai Cui Shaogang Wang Jihong Liu Ke Rao |
| author_sort | Rui Li |
| collection | DOAJ |
| description | Testosterone is overwhelmingly important in regulating erectile physiology. However, the associated molecular mechanisms are poorly understood. The purpose of this study was to explore the effects and mechanisms of testosterone in erectile dysfunction (ED) in castrated rats. Forty male Sprague-Dawley rats were randomized to four groups (control, sham-operated, castration and castration-with-testosterone-replacement). Reactive oxygen species (ROS) production was measured by dihydroethidium (DHE) staining. Erectile function was assessed by the recording of intracavernous pressure (ICP) and mean arterial blood pressure (MAP). Protein expression levels were examined by western blotting. We found that castration reduced erectile function and that testosterone restored it. Nitric oxide synthase (NOS) activity was decrease in the castrated rats, and testosterone administration attenuated this decrease (each p < 0.05). The testosterone, dihydrotestosterone, cyclic guanosine monophosphate (cGMP) and cyclic adenosine monophosphate (cAMP) concentrations were lower in the castrated rats, and testosterone restored these levels (each p < 0.05). Furthermore, the cyclooxygenase-2 (COX-2) and prostacyclin synthase (PTGIS) expression levels and phospho-endothelial nitric oxide synthase (p-eNOS, Ser1177)/endothelial nitric oxide synthase (eNOS) ratio were reduced in the castrated rats compared with the controls (each p < 0.05). In addition, the p40phox and p67phox expression levels were increased in the castrated rats, and testosterone reversed these changes (each p < 0.05). Overall, our results demonstrate that testosterone ameliorates ED after castration by reducing ROS production and increasing the activity of the eNOS/cGMP and COX-2/PTGIS/cAMP signaling pathways. |
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| last_indexed | 2024-03-09T08:07:08Z |
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| spelling | doaj.art-053be44a53854eb1b0cdf561a03843912023-12-02T23:45:23ZengPeerJ Inc.PeerJ2167-83592016-05-014e200010.7717/peerj.2000Testosterone improves erectile function through inhibition of reactive oxygen species generation in castrated ratsRui Li0Xianghu Meng1Yan Zhang2Tao Wang3Jun Yang4Yonghua Niu5Kai Cui6Shaogang Wang7Jihong Liu8Ke Rao9Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, ChinaDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, ChinaDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, ChinaDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, ChinaDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, ChinaDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, ChinaDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, ChinaDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, ChinaDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, ChinaDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, ChinaTestosterone is overwhelmingly important in regulating erectile physiology. However, the associated molecular mechanisms are poorly understood. The purpose of this study was to explore the effects and mechanisms of testosterone in erectile dysfunction (ED) in castrated rats. Forty male Sprague-Dawley rats were randomized to four groups (control, sham-operated, castration and castration-with-testosterone-replacement). Reactive oxygen species (ROS) production was measured by dihydroethidium (DHE) staining. Erectile function was assessed by the recording of intracavernous pressure (ICP) and mean arterial blood pressure (MAP). Protein expression levels were examined by western blotting. We found that castration reduced erectile function and that testosterone restored it. Nitric oxide synthase (NOS) activity was decrease in the castrated rats, and testosterone administration attenuated this decrease (each p < 0.05). The testosterone, dihydrotestosterone, cyclic guanosine monophosphate (cGMP) and cyclic adenosine monophosphate (cAMP) concentrations were lower in the castrated rats, and testosterone restored these levels (each p < 0.05). Furthermore, the cyclooxygenase-2 (COX-2) and prostacyclin synthase (PTGIS) expression levels and phospho-endothelial nitric oxide synthase (p-eNOS, Ser1177)/endothelial nitric oxide synthase (eNOS) ratio were reduced in the castrated rats compared with the controls (each p < 0.05). In addition, the p40phox and p67phox expression levels were increased in the castrated rats, and testosterone reversed these changes (each p < 0.05). Overall, our results demonstrate that testosterone ameliorates ED after castration by reducing ROS production and increasing the activity of the eNOS/cGMP and COX-2/PTGIS/cAMP signaling pathways.https://peerj.com/articles/2000.pdfTestosteroneReactive oxygen speciesCOX-2eNOSErectile dysfunction |
| spellingShingle | Rui Li Xianghu Meng Yan Zhang Tao Wang Jun Yang Yonghua Niu Kai Cui Shaogang Wang Jihong Liu Ke Rao Testosterone improves erectile function through inhibition of reactive oxygen species generation in castrated rats PeerJ Testosterone Reactive oxygen species COX-2 eNOS Erectile dysfunction |
| title | Testosterone improves erectile function through inhibition of reactive oxygen species generation in castrated rats |
| title_full | Testosterone improves erectile function through inhibition of reactive oxygen species generation in castrated rats |
| title_fullStr | Testosterone improves erectile function through inhibition of reactive oxygen species generation in castrated rats |
| title_full_unstemmed | Testosterone improves erectile function through inhibition of reactive oxygen species generation in castrated rats |
| title_short | Testosterone improves erectile function through inhibition of reactive oxygen species generation in castrated rats |
| title_sort | testosterone improves erectile function through inhibition of reactive oxygen species generation in castrated rats |
| topic | Testosterone Reactive oxygen species COX-2 eNOS Erectile dysfunction |
| url | https://peerj.com/articles/2000.pdf |
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