Evaluation of the protective effects of gossypin for ischemia/reperfusion injury in ovary tissue
Özet
Aim: Ovarian ischemia–reperfusion (I/R) injury is a serious gynecological condition that affects women of reproductive age and reduces ovarian reserve. Management of I/R injury with detorsion causes reperfusion damage, in which oxidative stress plays a central role. This study aimed to investigate whether the gossypin (GOS) with antioxidant properties, a flavonoid, has beneficial effects on the biochemical, molecular, and histopathological aspects of ovarian I/R injury. Methods: Thirty-three female Balb/c mice were randomly divided into five groups as follows: Healthy (Sham-operated control group), I/R (IR group), I/R + GOS 5 (I/R with GOS 5 mg/kg), I/R + GOS 10 (I/R with GOS 10 mg/kg), and I/R + GOS 20 (I/R with GOS 20 mg/kg). This was followed by 3 h of ischemia and subsequent reperfusion for 3 h after detorsion was exposed. GOS was injected 2 h before reperfusion. Results: IL-1β, IL-6, TNF-α, NF-κB, and CASP-3 mRNA expressions, SOD (superoxide dismutase) activity, GSH (glutathione), and MDA (malondialdehyde) levels, and histopathological changes were evaluated in ovarian tissue. Histological examination indicated that treatment of ovarian I/R injury with GOS led to the improvement of ovarian tissue, which was accompanied by an increase in SOD activity and GSH level and a decrease in MDA level, NF-κB, TNF-α, IL-1β, and IL-6 expressions. GOS was also corrected by reducing the elevated expression of CASP-3 as apoptosis-change marker. Conclusion: These findings indicate that the treatment of GOS may be useful as a conservative approach to reverse I/R injury via amelioration of oxidative stress parameters and histopathological scores, attenuation of inflammation, and the suppression of apoptosis. © 2021 Japan Society of Obstetrics and Gynecology.
Anahtar Kelimeler
Tam Kayıt
| Alan | Değer | Dil |
|---|---|---|
| dc.contributor.author | Dincer, Busra | |
| dc.contributor.author | Cinar, Irfan | |
| dc.contributor.author | Yayla, Muhammed | |
| dc.contributor.author | Toktay, Erdem | |
| dc.date.accessioned | 2026-10-18T20:27:47.629876969Z | |
| dc.date.available | 2026-10-18T20:27:47.629876969Z | |
| dc.date.issued | 2022 | |
| dc.description.abstract | Aim: Ovarian ischemia–reperfusion (I/R) injury is a serious gynecological condition that affects women of reproductive age and reduces ovarian reserve. Management of I/R injury with detorsion causes reperfusion damage, in which oxidative stress plays a central role. This study aimed to investigate whether the gossypin (GOS) with antioxidant properties, a flavonoid, has beneficial effects on the biochemical, molecular, and histopathological aspects of ovarian I/R injury. Methods: Thirty-three female Balb/c mice were randomly divided into five groups as follows: Healthy (Sham-operated control group), I/R (IR group), I/R + GOS 5 (I/R with GOS 5 mg/kg), I/R + GOS 10 (I/R with GOS 10 mg/kg), and I/R + GOS 20 (I/R with GOS 20 mg/kg). This was followed by 3 h of ischemia and subsequent reperfusion for 3 h after detorsion was exposed. GOS was injected 2 h before reperfusion. Results: IL-1β, IL-6, TNF-α, NF-κB, and CASP-3 mRNA expressions, SOD (superoxide dismutase) activity, GSH (glutathione), and MDA (malondialdehyde) levels, and histopathological changes were evaluated in ovarian tissue. Histological examination indicated that treatment of ovarian I/R injury with GOS led to the improvement of ovarian tissue, which was accompanied by an increase in SOD activity and GSH level and a decrease in MDA level, NF-κB, TNF-α, IL-1β, and IL-6 expressions. GOS was also corrected by reducing the elevated expression of CASP-3 as apoptosis-change marker. Conclusion: These findings indicate that the treatment of GOS may be useful as a conservative approach to reverse I/R injury via amelioration of oxidative stress parameters and histopathological scores, attenuation of inflammation, and the suppression of apoptosis. © 2021 Japan Society of Obstetrics and Gynecology. | |
| dc.identifier.doi | 10.1111/jog.15127 | |
| dc.identifier.eissn | 1447-0756 | |
| dc.identifier.endpage | 756 | |
| dc.identifier.issn | 1341-8076 | |
| dc.identifier.issue | 3 | |
| dc.identifier.pmid | 34931736 | |
| dc.identifier.scopus | 2-s2.0-85121466469 | |
| dc.identifier.startpage | 748 | |
| dc.identifier.uri | https://rdlopen.rawdatalibrary.net/r/ebyu/12941 | |
| dc.identifier.volume | 48 | |
| dc.identifier.wos | WOS:000731912000001 | |
| dc.language.iso | en | |
| dc.publisher | John Wiley and Sons Inc | |
| dc.relation.ispartof | Journal of Obstetrics and Gynaecology Research | |
| dc.rights | info:eu-repo/semantics/openAccess | |
| dc.subject | gossypin | |
| dc.subject | inflammation | |
| dc.subject | ischemia–reperfusion | |
| dc.subject | ovary | |
| dc.subject | oxidative stress | |
| dc.subject | Animals | |
| dc.subject | Antioxidants | |
| dc.subject | Female | |
| dc.subject | Flavonoids | |
| dc.subject | Ischemia | |
| dc.subject | Malondialdehyde | |
| dc.subject | Mice | |
| dc.subject | Rats | |
| dc.subject | Rats, Wistar | |
| dc.subject | Reperfusion Injury | |
| dc.subject | caspase 3 | |
| dc.subject | glutathione | |
| dc.subject | gossypine | |
| dc.subject | immunoglobulin enhancer binding protein | |
| dc.subject | interleukin 1beta | |
| dc.subject | interleukin 6 | |
| dc.subject | malonaldehyde | |
| dc.subject | messenger RNA | |
| dc.subject | superoxide dismutase | |
| dc.subject | tumor necrosis factor | |
| dc.subject | antioxidant | |
| dc.subject | flavonoid | |
| dc.subject | animal experiment | |
| dc.subject | animal model | |
| dc.subject | animal tissue | |
| dc.title | Evaluation of the protective effects of gossypin for ischemia/reperfusion injury in ovary tissue | |
| dc.type | Article | |
| dspace.entity.type | Publication | |
| rdl.citation.scopus | 13 | |
| rdl.citation.wos | 13 | |
| rdl.department | Faculty of Pharmacy, Department of Pharmacology, Erzincan Binali Yildirim University, Erzincan, Turkey. | |
| rdl.source.index | SCOPUS | |
| rdl.source.index | WOS | |
| rdl.source.index | PUBMED | |
| rdl.wos.index | Science Citation Index Expanded (SCI-EXPANDED) |
