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

作　　者：Xiao-mei HUANG E LIAO Jun-qun LIAO Ya-ling LIU Yong SHAO 

机构地区：[1]Department of Obstetrics and Gynecology,The First Affiliated Hospital of Chongqing Medical University,Chongqing 400042,China [2]Department of Obstetrics,Maternal and Child Health Hospital of Hubei Province,Wuhan 430070,China [3]Medical Laboratory Science,The First Affiliated Hospital of Chongqing Medical University,Chongqing 400042,China [4]Department of Obstetrics,Yubei Maternity and Child Healthcare Hospital,Chongqing 400042,China

出　　处：《Current Medical Science》2024年第1期187-194,共8页当代医学科学（英文）

摘　　要：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 epithelial-mesenchymal 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.

关 键 词：formyl peptide receptor 1 BOC-MLF epithelial-mesenchymal transition premature rupture of membranes 

分 类 号：R714[医药卫生—妇产科学]