Protective effects of ivermectin against ischemia-reperfusion-induced ovarian injury in rats
Abstract
BackgroundOvarian ischemia-reperfusion (I/R) injury induces severe tissue damage through oxidative stress and inflammation, and DNA damage. This study investigated the protective effects of short- and long-term ivermectin application against ovarian I/R injury in rats.MethodsTwenty-four female Wistar albino rats were divided into four groups: sham operation (SOG), ovarian I/R (OIR), long-term ivermectin-applied I/R (LIOIR), and short-term ivermectin-applied I/R (SIOIR). Ovarian torsion was maintained for 3 h before detorsion. Ivermectin (2 mg/kg, orally) was administered for 3 or 6 days. Ovarian malondialdehyde (MDA), total glutathione (tGSH), superoxide dismutase (SOD), and catalase (CAT) were measured. Histopathological and immunohistochemical analyses of cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), and 8-hydroxy-2′-deoxyguanosine (8-OHdG) were also performed.ResultsOIR increased MDA and reduced tGSH, SOD, and CAT. Three-day ivermectin pretreatment normalized oxidative stress marker levels to values comparable to those in the sham group, whereas six-day pretreatment provided no significant protection. Follicular degeneration was pronounced in OIR and LIOIR but markedly attenuated in SIOIR. Immunohistochemistry demonstrated preserved COX-1 expression and reduced COX-2 and 8-OHdG immunoreactivity following short-term ivermectin pretreatment.ConclusionShort-term ivermectin effectively protected ovarian tissue against experimental I/R injury by reducing oxidative stress, inflammation, and DNA damage, whereas prolonged pretreatment failed to provide comparable protection, supporting its therapeutic potential.
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BibTeX
@article{yilmaz2026protective,
title = {{Protective effects of ivermectin against ischemia-reperfusion-induced ovarian injury in rats}},
author = {Nesrin Yilmaz and Seval Bulut and Seyma Ilayda Paltaci and Renad Mammadov and Cengiz Sarigul and Mustafa Ozkaraca and Behzat Tebrizi and Halis Suleyman},
journal = {Frontiers in Pharmacology},
year = {2026},
month = nov,
doi = {10.3389/fphar.2026.2003125},
url = {https://www.frontiersin.org/articles/10.3389/fphar.2026.2003125},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Protective effects of ivermectin against ischemia-reperfusion-induced ovarian injury in rats
AU - Nesrin Yilmaz
AU - Seval Bulut
AU - Seyma Ilayda Paltaci
AU - Renad Mammadov
AU - Cengiz Sarigul
AU - Mustafa Ozkaraca
AU - Behzat Tebrizi
AU - Halis Suleyman
PY - 2026
DA - 2026/11/04
JO - Frontiers in Pharmacology
DO - 10.3389/fphar.2026.2003125
UR - https://www.frontiersin.org/articles/10.3389/fphar.2026.2003125
AB - BackgroundOvarian ischemia-reperfusion (I/R) injury induces severe tissue damage through oxidative stress and inflammation, and DNA damage. This study investigated the protective effects of short- and long-term ivermectin application against ovarian I/R injury in rats.MethodsTwenty-four female Wistar albino rats were divided into four groups: sham operation (SOG), ovarian I/R (OIR), long-term ivermectin-applied I/R (LIOIR), and short-term ivermectin-applied I/R (SIOIR). Ovarian torsion was maintained for 3 h before detorsion. Ivermectin (2 mg/kg, orally) was administered for 3 or 6 days. Ovarian malondialdehyde (MDA), total glutathione (tGSH), superoxide dismutase (SOD), and catalase (CAT) were measured. Histopathological and immunohistochemical analyses of cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), and 8-hydroxy-2′-deoxyguanosine (8-OHdG) were also performed.ResultsOIR increased MDA and reduced tGSH, SOD, and CAT. Three-day ivermectin pretreatment normalized oxidative stress marker levels to values comparable to those in the sham group, whereas six-day pretreatment provided no significant protection. Follicular degeneration was pronounced in OIR and LIOIR but markedly attenuated in SIOIR. Immunohistochemistry demonstrated preserved COX-1 expression and reduced COX-2 and 8-OHdG immunoreactivity following short-term ivermectin pretreatment.ConclusionShort-term ivermectin effectively protected ovarian tissue against experimental I/R injury by reducing oxidative stress, inflammation, and DNA damage, whereas prolonged pretreatment failed to provide comparable protection, supporting its therapeutic potential.
SN - 1663-9812
ER -