https://orcid.org/0000-0003-4730-5015
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Abstract
Objective
Ovarian ischemia constitutes 2–3% of all gynecological emergencies. New-generation therapeutic agents need to be discovered, in addition to invasive interventions capable of reducing the risk of potential ovarian ischemia to a minimum and protecting against potential adverse outcomes.
Aims
To investigate the effects of amiodarone (AMD) on ischemia-reperfusion-induced oxidative stress and inflammation-induced ovarian damage.
Methods
The control group, received intraperitoneal (i.p.) injection of saline solution. The ischemia group (I-Group), was subjected to ischemia-induced injury without drug administration. The ischemia + AMD (50 mg/kg) group was subjected to ischemia injury and also received i.p. 50 mg/kg AMD prior to induction of ovarian ischemia. The ischemia–reperfusion (I/R group) was exposed to ischemia and reperfusion-induced injury without drug administration. The I/R + AMD (50 mg/kg) group underwent I/R injury together with i.p. administration of 50 mg/kg AMD prior to induction of ovarian I/R. The Sham + AMD group received intraperitoneal (i.p.) injection of 50 mg/kg AMD alone. In this study performed thiobarbituric acid reactive substances (TBARS), thiol (−SH), interleukin 1 Beta (IL-1β), interleukin 6 (IL-6), toll-like receptor 4 (TLR4) and nuclear factor-kappa B(NF-κβ).
Results
Increased oxidative stress and inflammation as a result of ovarian I and I/R application activated the cascade. AMD was not sufficient to reduce the oxidative stress and inflammation. TLR4 and NF-kβ, which were up-regulated by triggering oxidative stress and inflammation, were not regressed by the effects of AMD.
Conclusions
AMD, used as an antiarrhythmic agent, was found to be insufficient, despite its antioxidant and anti-inflammatory properties, to reduce the experimentally induced ovarian tissue damage.
Disclosure statement
No potential conflict of interest was reported by the author(s).