Lipopolysaccharide-Induced pregnant mice had decreased serum iron while maintaining hepcidin level and Hamp1 mRNA expression
Abstract
Hepcidin is a hormone that regulates systemic iron homeostasis and is mostly produced in the liver. In pregnant women with inflammation, there are two opposing mechanisms in hepcidin expression: the suppression of hepcidin synthesis by pregnancy and the induction of hepcidin by inflammation. These conditions must receive special attention so that clinicians can give proper treatment and management to pregnant women with inflammation. Therefore, this study aims to prove changes in hepcidin and serum iron levels in pregnant mice with inflammation. This study involved sixteen second week pregnant mice which were divided into two groups. Pregnant mice were injected with lipopolysaccharide (LPS) Escherichia coli serotype O111:B4 as much as 1 µg/g body weight intraperitoneally as the treatment group, while pregnant mice were injected with phosphate buffer saline (PBS) as a control group. Serum was measured using ELISA to determine hepcidin levels and colorimetry to determine serum iron. Mice livers were measured using Real Time PCR to determine Hamp1 mRNA expression. The data obtained were analyzed using an independent t-test. Our results show that pregnant mice with inflammation show that there was no difference in Hamp1 mRNA expression (p-value=0.163) and hepcidin level (p-value=0.789), but there was a significant difference in serum iron level (p-value=0.035). This study demonstrates that inflammation in pregnancy does not affect changes in Hamp1 expression and hepcidin level, but reduces serum iron, which could be caused by regulation of hepcidin in the fetus.
Keywords: Inflammation, Hamp1, Hepcidin, Pregnancy, Serum iron
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