The suppressive effects of Simvastatin on fertility impairment induced by experimental unilateral testicular ischemia-reperfusion in mice
178 Background: The basic pathophysiologic phenomenon in testicular torsion, a common urologic emergency, is ischemia followed by reperfusion. In this study, we evaluated the effect(s) of simvastatin (SIM), a lipid lowering agent with antioxidant and anti-inflammatory properties, on mouse epididyma...
Main Authors: | , , , , , |
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Format: | Article |
Language: | English |
Published: |
Babol University of Medical Sciences
2016-12-01
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Series: | Caspian Journal of Reproductive Medicine |
Subjects: | |
Online Access: | http://caspjrm.ir/article-1-113-en.html |
Summary: | 178
Background: The basic pathophysiologic phenomenon in testicular torsion, a common urologic emergency, is ischemia followed by reperfusion. In this study, we evaluated the effect(s) of simvastatin (SIM), a lipid lowering agent with antioxidant and anti-inflammatory properties, on mouse epididymal sperm fertilizing potential and the subsequent in vitro embryo development in experimentally-induced unilateral testicular ischemia-reperfusion (IR).
Methods: Adult male mice were divided into four groups (n = 6, each). Following anaesthesia, IR was induced by clamping the left testicular vessels with an atraumatic microvascular clamp for 30 minutes in the IR group. In IR+SIM group, in addition, the mice received SIM (20 mg/kg per day) orally for 3 days starting from the day of induction of the experimental IR. A vehicle-treated control group and a SIM-only treated group were also included. Ipsilateral and contralateral epididymal sperms fertilizing capacity was analyzed in four groups after 35 days.
Results: Significant reduction in fertilization as well as blastulation rates were observed in the IR group. However, the SIM treatment considerably attenuated the IR-induced negative alterations in the above-mentioned parameters.
Conclusion: These findings revealed the repro-protective effects of SIM on the murine model of IR through the inhibition of oxidative injuries and inflammatory reactions. |
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ISSN: | 2423-5660 2423-5660 |