Abstract

Introduction: The expression of hepcidin in hepatocytes is induced by inflammation, primarily mediated by interleukin 6 (IL-6) and activin B. In contrast, hepcidin levels are suppressed during pregnancy via the half-site of the estrogen-responsive element (ERE) on the hepcidin gene promoter. These opposing mechanisms regulate hepcidin in pregnant women with inflammation. However, several studies report no change in hepcidin levels in the blood of pregnant women experiencing inflammation. Therefore, this study investigated the expression of hepcidin in pregnant mice with induced inflammation using LPS injection. Materials and methods: This study involved 26 pregnant mice. The treatment group was injected intraperitoneally with serotype O111:B4 (Sigma-Aldrich, Merck, Singapore), while the control group received Phosphate Buffered Saline (PBS). Serum levels of IL-6, activin B, estradiol, and hepcidin were measured using ELISA. The liver tissues were examined via immunohistochemistry to measure the Transforming Growth Factor-β (TGF-β) receptor. Data were analyzed using an independent t-test. Results: Our results demonstrated that pregnant mice with inflammation had significantly increased IL-6 (P = 0.000) and decreased activin B (P = 0.032) levels, but there were no significant differences in estradiol (P = 0.624), hepcidin (P = 0.607), and TGF-β receptor levels (P=0.662). Conclusion: Our study showed that inflammation during pregnancy does not impact hepcidin levels. Additionally, we observed a decrease in activin B levels in pregnant mice with inflammation. Conversely, high levels of estradiol during pregnancy may contribute to the suppression of hepcidin synthesis.

Original languageEnglish
Pages (from-to)38-43
Number of pages6
JournalMalaysian Journal of Medicine and Health Sciences
Volume20
Issue number6
DOIs
Publication statusPublished - Nov 2024

Keywords

  • Activin B
  • Estradiol
  • Hepcidin
  • Inflammation
  • Interleukin-6
  • Pregnancy

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