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Published on: March 11, 2018
Sesamol Protects Testis from Ischemia-Reperfusion Injury through Scavenging Reactive Oxygen Species and Upregulating
Si-Ming Wei1,2, Rong-Yun Wang2, Yan-Song Chen3,4
1Shulan International Medical College, Zhejiang Shuren University, Hangzhou City, Zhejiang Province 310015, China.
Abstract:
Testicular torsion/detorsion-induced damage is considered as a typical ischemia-reperfusion injury attributed to excessive reactive oxygen species (ROS) production. ROS may regulate many genes whose expression affects cell-cycle regulation, cell proliferation, and apoptosis. The cAMP-responsive element modulator-τ (CREMτ) gene expression in the testis is essential for normal germ cell differentiation. The present study was aimed at investigating the effect of sesamol, a powerful antioxidant, on testicular ischemia-reperfusion injury and related mechanisms in an experimental testicular torsion-detorsion rat model. The type of our study was a randomized controlled trial. Sixty rats were randomly divided into the following 3 groups: (1) sham-operated control group (n = 20), (2) testicular ischemia-reperfusion group (n = 20), and (3) testicular ischemia-reperfusion+sesamol-treated group (n = 20). Testicular ischemia-reperfusion was induced by left testicular torsion (720° rotation in a counterclockwise direction) for 2 hours, followed by detorsion. Orchiectomy was performed at 4 hours or 3 months after detorsion. The testis was obtained for the analysis of the following parameters, including malondialdehyde level (a sensitive indicator of ROS), CREMτ expression, and spermatogenesis. In the testicular ischemia-reperfusion group, the malondialdehyde level was significantly increased with a concomitant significant decrease in CREMτ expression and spermatogenesis in ipsilateral testis. These results suggest that overproduction of ROS after testicular ischemia-reperfusion may downregulate CREMτ expression, which causes spermatogenic injury. Sesamol treatment resulted in a significant reduction in the malondialdehyde level and significant increase in CREMτ expression and spermatogenesis in ipsilateral testis. These data support the above suggestion. Our study shows that sesamol can attenuate testicular ischemia-reperfusion injury through scavenging ROS and upregulating CREMτ expression.
Insights
Testicular torsion causes damage via reactive oxygen species (ROS). Sesamol, an antioxidant, protected against this injury by reducing ROS and improving sperm production by upregulating CREMτ expression.
Area of Science:
- Reproductive Medicine
- Oxidative Stress Research
- Biochemistry
Background:
- Testicular torsion/detorsion causes ischemia-reperfusion injury, linked to excessive reactive oxygen species (ROS).
- ROS impacts cell cycle, proliferation, and apoptosis.
- cAMP-responsive element modulator-τ (CREMτ) gene expression is vital for germ cell differentiation.
Purpose of the Study:
- To investigate the protective effects of sesamol, a potent antioxidant, against testicular ischemia-reperfusion injury.
- To explore the underlying mechanisms involving ROS and CREMτ expression in a rat model.
Main Methods:
- A randomized controlled trial involving 60 rats divided into sham-operated, ischemia-reperfusion, and sesamol-treated groups.
- Testicular ischemia-reperfusion induced by 2-hour torsion followed by detorsion.
- Analysis of malondialdehyde (ROS indicator), CREMτ expression, and spermatogenesis at 4 hours and 3 months post-detorsion.
Main Results:
- Ischemia-reperfusion significantly increased malondialdehyde levels and decreased CREMτ expression and spermatogenesis.
- Sesamol treatment significantly reduced malondialdehyde levels.
- Sesamol administration led to a significant increase in CREMτ expression and improved spermatogenesis.
Conclusions:
- Excessive ROS production following testicular ischemia-reperfusion downregulates CREMτ expression, leading to spermatogenic damage.
- Sesamol attenuates testicular ischemia-reperfusion injury by scavenging ROS.
- Sesamol upregulates CREMτ expression, thereby protecting against testicular injury and preserving spermatogenesis.
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