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Objective: Premature rupture of membranes (PROM) is a common pregnancy disorder that is closely associated with structural weakening of fetal membranes. Studies have found that formyl peptide receptor 1 (FPR1) activates inflammatory pathways and amniotic epithelialmesenchymal transition (EMT), stimulates collagen degradation, and leads to membrane weakening and membrane rupture. The purpose of this study was to investigate the anti-inflammatory and EMT inhibitory effects of FPR1 antagonist (BOC-MLF) to provide a basis for clinical prevention of PROM.

Methods: The relationship between PROM, FPR1, and EMT was analyzed in human fetal membrane tissue and plasma samples using Western blotting, PCR, Masson staining, and ELISA assays. Lipopolysaccharide (LPS) was used to establish a fetal membrane inflammation model in pregnant rats, and BOC-MLF was used to treat the LPS rat model. We detected interleukin (IL)-6 in blood from the rat hearts to determine whether the inflammatory model was successful and whether the anti-inflammatory treatment was effective. We used electron microscopy to analyze the structure and collagen expression of rat fetal membrane.

Results: Western blotting, PCR and Masson staining indicated that the expression of FPR1 was significantly increased, the expression of collagen was decreased, and EMT appeared in PROM. The rat model indicated that LPS caused the collapse of fetal membrane epithelial cells, increased intercellular gaps, and decreased collagen. BOC-MLF promoted an increase in fetal membrane collagen, inhibited EMT, and reduced the weakening of fetal membranes.

Conclusion: The expression of FPR1 in the fetal membrane of PROM was significantly increased, and EMT of the amniotic membrane was obvious. BOC-MLF can treat inflammation and inhibit amniotic EMT.

Titel:	FPR1 Antagonist (BOC-MLF) Inhibits Amniotic Epithelial-mesenchymal Transition.
Autor/in / Beteiligte Person:	Huang, XM ; Liao, E ; Liao, JQ ; Liu, YL ; Shao, Y
Link:	View record at Springer (Volltext)
Zeitschrift:	Current medical science, Jg. 44 (2024-02-01), Heft 1, S. 187-194
Veröffentlichung:	Wuhan : Huazhong University of Science and Technology, [2018]-, 2024
Medientyp:	academicJournal
ISSN:	2523-899X (electronic)
DOI:	10.1007/s11596-023-2794-6
Schlagwort:	Pregnancy Female Humans Animals Rats Receptors, Formyl Peptide genetics Receptors, Formyl Peptide metabolism Inflammation drug therapy Inflammation metabolism Collagen metabolism Anti-Inflammatory Agents Epithelial-Mesenchymal Transition Amnion metabolism Lipopolysaccharides pharmacology
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article Language: English [Curr Med Sci] 2024 Feb; Vol. 44 (1), pp. 187-194. <i>Date of Electronic Publication: </i>2024 Feb 01. MeSH Terms: Amnion* / metabolism ; Lipopolysaccharides* / pharmacology ; Pregnancy ; Female ; Humans ; Animals ; Rats ; Receptors, Formyl Peptide / genetics ; Receptors, Formyl Peptide / metabolism ; Inflammation / drug therapy ; Inflammation / metabolism ; Collagen / metabolism ; Anti-Inflammatory Agents ; Epithelial-Mesenchymal Transition References: Schmitz T, Sentilhes L, Lorthe E, et al. Preterm premature rupture of the membranes: Guidelines for clinical practice from the French College of Gynaecologists and Obstetricians (CNGOF). Eur J Obstet Gynecol Reprod Biol, 2019,236:1–6. (PMID: 10.1016/j.ejogrb.2019.02.02130870741) ; Practice Bulletin No. 172: Premature Rupture of Membranes. Obstet Gynecol, 2016,128(4):e165–e177. ; Pasquier JC, Doret M. 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(PMID: 10.1016/j.freeradbiomed.2017.02.03828232203) Contributed Indexing: Keywords: BOC-MLF; epithelial-mesenchymal transition; formyl peptide receptor 1; premature rupture of membranes Substance Nomenclature: 0 (Lipopolysaccharides) ; 0 (Receptors, Formyl Peptide) ; 9007-34-5 (Collagen) ; 0 (Anti-Inflammatory Agents) ; 0 (FPR1 protein, human) Entry Date(s): Date Created: 20240201 Date Completed: 20240226 Latest Revision: 20240226 Update Code: 20240226

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FPR1 Antagonist (BOC-MLF) Inhibits Amniotic Epithelial-mesenchymal Transition.