Carvacrol treatment opens Kir6.2 ATP-dependent potassium channels and prevents apoptosis on rat testis following ischemia-reperfusion injury model.


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Balci C. N., Firat T., Acar N., Kukner A.

Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie, cilt.62, sa.1, ss.179-190, 2021 (SCI-Expanded) identifier

Özet

Testicular torsion is a urological problem that causes subfertility and testicular damage in males. Testis torsion and detorsion lead to ischemia–

reperfusion (IR) injury in the testis. Testicular IR injury causes the increase of reactive oxygen species (ROS), oxidative stress (OS) and germ

cell-specific apoptosis. In this study, we aimed to investigate whether Carvacrol has a protective effect on testicular IR injury and its effects

on Kir6.2 channels, which is a member of adenosine triphosphate (ATP)-dependent potassium channels. In the study, 2–4 months old 36

albino Wistar rats were used. For experimental testicular IR model, the left testis was rotated counterclockwise at 720º for two hours, and

after two hours following torsion, detorsion was performed. Carvacrol was dissolved in 5% Dimethyl Sulfoxide (DMSO) at a dose of 73 mg/kg

and half an hour before detorsion, 0.2 mL was administered intraperitoneally. In testicular tissues, caspase 3 and Kir6.2 immunoexpressions

were examined. Serum malondialdehyde (MDA) and testosterone levels were measured. Apoptotic cells and serum MDA levels were

significantly decreased and Kir6.2 activation was significantly increased in Carvacrol-administrated IR group. As a result of our study,

Carvacrol may activates Kir6.2 channels and inhibits apoptosis and may have a protective effect on testicular IR injury.