ArticlePeerJ2016
Testosterone improves erectile function through inhibition of reactive oxygen species generation in castrated rats.
Article in PeerJ, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 45 citations in OpenAlex.
- Chronic administration of the hydrogen sulfide prodrug SG1002 partially protects against erectile dysfunction resulting from long-term androgen deprivation.Life sciences · 2025Article
- Zhenyuan, a kidney- and spleen-tonifying Chinese medicine compound granule, improves erectile dysfunction and fatigue in orchiectomized rats.Translational andrology and urology · 2025Article
- Testosterone improved erectile function by upregulating transcriptional expression of growth factors in late androgen replacement therapy model rats.International journal of impotence research · 2024Article
- Low androgen levels induce ferroptosis of rat penile cavernous endothelial cells.Sexual medicine · 2023Article
- Article
- Ex vivo Akt inhibition reverses castration induced internal pudendal artery and penile endothelial dysfunction.Life sciences · 2021Article
- Effect of Late Androgen Replacement Therapy on Erectile Function Through Structural Changes in Castrated Rats.Sexual medicine · 2021Article
- Calorie Restriction Protects against Contrast-Induced Nephropathy via SIRT1/GPX4 Activation.Oxidative medicine and cellular longevity · 2021Article
- Influences of Sex and Estrogen in Arterial and Valvular Calcification.Frontiers in endocrinology · 2019Review
- Androgen Deficiency and Phosphodiesterase Type 5 Expression Changes in Aging Male: Therapeutic Implications.Frontiers in endocrinology · 2019Review
- Curcumin ameliorates atrophy of seminal vesicle via reduction of oxidative stress in castrated mice.PeerJ · 2019Article
- Article
- Downregulated Expression of Solute Carrier Family 26 Member 6 in NRK-52E Cells Attenuates Oxalate-Induced Intracellular Oxidative Stress.Oxidative medicine and cellular longevity · 2018Article
- Metabolic syndrome in rats is associated with erectile dysfunction by impairing PI3K/Akt/eNOS activity.Scientific reports · 2017Article
- Pathophysiology of Aortic Valve Stenosis: Is It Both Fibrocalcific and Sex Specific?Physiology (Bethesda, Md.) · 2017Review
- Involvement of DDAH/ADMA/NOS/cGMP and COX-2/PTGIS/cAMP Pathways in Human Tissue Kallikrein 1 Protecting Erectile Function in Aged Rats.PloS one · 2017Article
- Comparative evaluation of the sexual functions and NF-κB and Nrf2 pathways of some aphrodisiac herbal extracts in male rats.BMC complementary and alternative medicine · 2016Article
- Human tissue kallikrein-1 protects against the development of erectile dysfunction in a rat model of hyperhomocysteinemia.Asian journal of andrologyArticle
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 p40(phox) and p67(phox) 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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.