Controlled reperfusion for different durations in the treatment of ischemia-reperfusion injury of the rat ovary: evaluation of biochemical features, molecular gene expression, and histopathology.
High numbers of proinflammatory cells (PMNLs), which are carried by the blood to ischemic tissue during reperfusion, are considered responsible for inducing the inflammatory response that occurs in ischemia-reperfusion (I/R) injury. Our objective was to determine the controlled reperfusion (CR) interval duration (CRID) that would minimize the injury caused by the PMNLs that infiltrate ischemic tissue. Animal groups were divided into the following groups: Sham group, ovarian I/R group (OIR), and ovarian ischemia controlled-reperfusion groups OICR-1, OICR-2, OICR-3, OICR-4, OICR-5, OICR-6, which had their ovarian artery opened and then closed for 10, 8, 6, 4, 2, or 1 s, respectively. The results show that the COX-2 activity and the gene expression decreased while the COX-1 activity and the gene expression were found to be increased in parallel to the shortening of the period in CRID. From the histopathological examinations, the findings of hemorrhage, edema, congested vascular structures, degenerated cells, and migration and adhesion of PMNLs were scaled as follows: Sham group < OICR-6 < OICR-5 < OICR-4 < OICR-3 < OICR-2 < OICR-1. The results from the histopathological assessments were consistent with the molecular and biochemical findings. In conclusion, our findings suggest that increased COX-2 activity plays a role in I/R injury of the rat ovary, and that controlled reperfusion for 3, 2, or 1 s following 2 h of ischemia may attenuate the effects of I/R injury.
Department of Obstetrics and Gynecology, Faculty of Medicine, Ataturk University, Erzurum 25250, Turkey.
Omer Erkan
OE
Yapca
Serkan
S
Kumbasar
Suleyman
S
Salman
Oguzhan
O
Yarali
Ebru
E
Sener
Renad
R
Mammadov
Yesim Bayoglu
YB
Tekin
Aysenur
A
Aksoy
Abdulmecit
A
Albayrak
Nihal
N
Cetin
D000818:Animals; D002448:Cell Adhesion; D051545:Cyclooxygenase 1 / Q000235:genetics / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D004487:Edema / Q000209:etiology / Q000517:prevention & control; D005260:Female; D015971:Gene Expression Regulation, Enzymologic; D006470:Hemorrhage / Q000209:etiology / Q000517:prevention & control; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism; D020556:Neutrophil Infiltration; D009504:Neutrophils / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D009869:Oophoritis / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D010053:Ovary / Q000098:blood supply* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D017208:Rats, Wistar; D015424:Reperfusion; D015427:Reperfusion Injury / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D013997:Time Factors
D008565:Membrane Proteins; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; C496513:Ptgs1 protein, rat; C489691:Ptgs2 protein, rat
COX-1; COX-2; PMN; PMNL; antioxidants; antioxydants; hemorrhage; hémorragie