{"title":"Fractalkine/CX3CL1 and macrophage inflammatory protein- 1β/CCL4 activity in the rat ovary with induced ovarian hyperstimulation.","authors":"Gülcan Akverdi, Şehmus Pala, Remzi Atılgan, Tuncay Kuloğlu, Serhat Hançer, Nevin İlhan","doi":"10.4274/tjod.galenos.2024.72002","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>Fractalkine (CX3CL1) and macrophage inflammatory protein-1β (MIP-1β)/CCL4 play a role in chemotactic activity, immune response, and inflammatory response. We aimed to investigate the effects of fractalkine and MIP-1β in the development of ovarian hyperstimulation syndrome (OHSS) by considering the inflammatory response during ovulation.</p><p><strong>Materials and methods: </strong>Two equal groups of 20 immature female rats were created. Given that one of the rats in the group died, the control group was made up of 9 rats. Group 1 (G1) (n=9): Control group; G2 (n=10): OHSS group. Rats in the G2 group were administered 10 IU FSH for 4 days and 30 IU human chorionic gonadotropin on the fifth day. At 34 days old, all rats were sacrificed, and blood and ovarian tissue samples were collected to measure CX3CL1, CX3CL1R, MIP- 1β, tumor necrosis factor-alpha (TNF-α), interleukin (IL-8), hypoxia-inducible factor (HIF-1α), and interferon-gamma (IFN-γ) levels. Immunohistochemical scoring was performed for CX3CL1 and CX3CL1R in other ovarian tissue.</p><p><strong>Results: </strong>Rat and ovary weights and serum CX3CL1, CX3CLR1, HIF-1α, MIP-1β, TNF-α, IFN-γ and IL-8 levels were significantly higher in G2 than in G1. Tissue IL-8, TNF-α, CX3CL1, CX3CLR1, MIP-1β levels and CX3CL1 and CX3CLR1 immunoreactivity scores were significantly higher in G2 than in G1.</p><p><strong>Conclusion: </strong>CX3CL1 and MIP-1β contribute to the pathophysiology of OHSS by playing a role in the development of inflammation.</p>","PeriodicalId":45340,"journal":{"name":"Turkish Journal of Obstetrics and Gynecology","volume":"21 4","pages":"220-226"},"PeriodicalIF":1.0000,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11635723/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Turkish Journal of Obstetrics and Gynecology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4274/tjod.galenos.2024.72002","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"OBSTETRICS & GYNECOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: Fractalkine (CX3CL1) and macrophage inflammatory protein-1β (MIP-1β)/CCL4 play a role in chemotactic activity, immune response, and inflammatory response. We aimed to investigate the effects of fractalkine and MIP-1β in the development of ovarian hyperstimulation syndrome (OHSS) by considering the inflammatory response during ovulation.
Materials and methods: Two equal groups of 20 immature female rats were created. Given that one of the rats in the group died, the control group was made up of 9 rats. Group 1 (G1) (n=9): Control group; G2 (n=10): OHSS group. Rats in the G2 group were administered 10 IU FSH for 4 days and 30 IU human chorionic gonadotropin on the fifth day. At 34 days old, all rats were sacrificed, and blood and ovarian tissue samples were collected to measure CX3CL1, CX3CL1R, MIP- 1β, tumor necrosis factor-alpha (TNF-α), interleukin (IL-8), hypoxia-inducible factor (HIF-1α), and interferon-gamma (IFN-γ) levels. Immunohistochemical scoring was performed for CX3CL1 and CX3CL1R in other ovarian tissue.
Results: Rat and ovary weights and serum CX3CL1, CX3CLR1, HIF-1α, MIP-1β, TNF-α, IFN-γ and IL-8 levels were significantly higher in G2 than in G1. Tissue IL-8, TNF-α, CX3CL1, CX3CLR1, MIP-1β levels and CX3CL1 and CX3CLR1 immunoreactivity scores were significantly higher in G2 than in G1.
Conclusion: CX3CL1 and MIP-1β contribute to the pathophysiology of OHSS by playing a role in the development of inflammation.