Capsaicin protects against testicular torsion injury through mTOR-dependent mechanism

Testicular torsion and subsequent release of reactive oxygen species (ROS) can cause infertility in adults. Oxidative stress following testicular torsion plays an important role in the ýonset and development of apoptotic cell death through dysregulation of the cellular signaling pathways. Anti-infla...

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Veröffentlicht in:Theriogenology 2018-06, Vol.113, p.247-252
Hauptverfasser: Javdan, Nasim, Ayatollahi, Seyed Abdulmajid, Choudhary, Muhammad Iqbal, Al-Hasani, Safaa, Kobarfard, Farzad, Athar, Ata, Pazoki-Toroudi, Hamidreza
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Sprache:eng
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Zusammenfassung:Testicular torsion and subsequent release of reactive oxygen species (ROS) can cause infertility in adults. Oxidative stress following testicular torsion plays an important role in the ýonset and development of apoptotic cell death through dysregulation of the cellular signaling pathways. Anti-inflammatory and antioxidant properties of capsaicin, a bioactive composition present in red peppers, has already been exploited for treatment of the cancer and pain relief. In present work, we evaluated the role of the mammalian target of rapamycin (mTOR) in antioxidant effect of capsaicin against reperfusion injury following testicular torsion. Male Wistar rats weighing 200–220 g were randomly assigned into four major groups: (i) a sham operated group, (ii) a testicular torsion (TT) group, (iii) three groups treated with different doses of capsaicin (TT + 100, 500 and 1000 μg/ml Cap), and (iv) three groups of healthy rats treated with different doses of capsaicin (100, 500 and 1000 μg/ml). Western blotting assay was used to examine the anti-apoptotic effects of capsaicin in testicular cells following torsion. H&E and TUNEL methods were used to evaluate testicular morphology and apoptosis activity. Compared to control group, phosphorylation of mTOR was significantly increased in the TT groups. Capsaicin administration remarkably decreased the phosphorylation of mTOR at the highest dose (P 
ISSN:0093-691X
1879-3231
DOI:10.1016/j.theriogenology.2018.03.012