TY - JOUR
T1 - The Effect of Lipopolysaccharide Exposure During Pregnancy on Hepcidin Expression in Female Mice
T2 - Involvement of Interleukin-6 and Activin B, Independent of Transforming Growth Factor-β Receptor
AU - Nugraha, Gilang
AU - Widjiati,
AU - Aryati,
AU - Wungu, Citrawati Dyah Kencono
AU - Notopuro, Harianto
AU - Darmanto, Win
AU - Sulistyono, Agus
AU - Notobroto, Hari Basuki
AU - Rejeki, Purwo Sri
N1 - Publisher Copyright:
© 2024 Universiti Putra Malaysia Press. All rights reserved.
PY - 2024/11
Y1 - 2024/11
N2 - 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.
AB - 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.
KW - Activin B
KW - Estradiol
KW - Hepcidin
KW - Inflammation
KW - Interleukin-6
KW - Pregnancy
UR - http://www.scopus.com/inward/record.url?scp=85210918415&partnerID=8YFLogxK
U2 - 10.47836/mjmhs.20.6.7
DO - 10.47836/mjmhs.20.6.7
M3 - Article
AN - SCOPUS:85210918415
SN - 1675-8544
VL - 20
SP - 38
EP - 43
JO - Malaysian Journal of Medicine and Health Sciences
JF - Malaysian Journal of Medicine and Health Sciences
IS - 6
ER -