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孕酮通过减轻牙源性诱导的小鼠慢性炎症来抑制子宫收缩。

Progesterone Suppresses Uterine Contraction by Reducing Odontogenic Induced Chronic Inflammation in Mice.

作者信息

Teraoka Yuko, Sugimoto Jun, Konishi Haruhisa, Miyoshi Hiroshi, Furusho Hisako, Miyauchi Mutsumi, Kajioka Shunichi, Koh Iemasa, Kudo Yoshiki

机构信息

Department of Obstetrics and Gynecology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima 734-8551, Japan.

Department of Obstetrics and Gynecology, Miyoshi Central Hospital, Miyoshi 728-8502, Japan.

出版信息

Biomolecules. 2022 Jul 26;12(8):1029. doi: 10.3390/biom12081029.

DOI:10.3390/biom12081029
PMID:35892338
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9332501/
Abstract

Preterm birth is one of the most significant obstetric complications. Inflammation reportedly promotes uterine contraction and weakening of the fetal membrane, which induces preterm birth. Previous studies using animal models of lipopolysaccharide-induced acute inflammation have shown that progesterone (P4) promotes uterine quiescence. However, this effect is not fully understood in chronic inflammation. This study aimed to investigate the effects of P4 on uterine contractility and inflammation of the fetal membrane in mice infected with (), a major periodontal pathogen as a model of preterm birth caused by chronic inflammation. Mice were injected with 1 mg of P4 from day 15.5 to 17.5. P4 prolonged the mean gestation period of mice from 18.3 to 20.4 days, and no reduction in the gestation period was observed. P4 treatment suppressed spontaneous uterine contractility and decreased oxytocin sensitivity. In addition, the expression of inflammatory cytokines in the fetal membrane was significantly reduced. Thus, P4 prevented preterm birth by suppressing enhanced uterine contractility induced by chronic inflammation in this model. This result describes the effects of P4 in a chronic inflammation model, which may lead to a better understanding of the efficacy of P4 in preventing preterm birth in humans.

摘要

早产是最严重的产科并发症之一。据报道,炎症会促进子宫收缩和胎膜变薄,从而引发早产。此前使用脂多糖诱导急性炎症动物模型的研究表明,孕酮(P4)可促进子宫静止。然而,在慢性炎症中,这种作用尚未完全明确。本研究旨在探讨P4对感染牙龈卟啉单胞菌(一种主要的牙周病原体,作为慢性炎症导致早产的模型)的小鼠子宫收缩性和胎膜炎症的影响。从第15.5天至17.5天给小鼠注射1毫克P4。P4使小鼠的平均妊娠期从18.3天延长至20.4天,未观察到妊娠期缩短。P4治疗可抑制子宫自发性收缩,并降低催产素敏感性。此外,胎膜中炎性细胞因子的表达显著降低。因此,在该模型中,P4通过抑制慢性炎症诱导的子宫收缩增强来预防早产。这一结果描述了P4在慢性炎症模型中的作用,可能有助于更好地理解P4在预防人类早产方面的功效。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc7b/9332501/d26db8f83616/biomolecules-12-01029-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc7b/9332501/cce5d91c108e/biomolecules-12-01029-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc7b/9332501/d26db8f83616/biomolecules-12-01029-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc7b/9332501/cce5d91c108e/biomolecules-12-01029-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc7b/9332501/d26db8f83616/biomolecules-12-01029-g002.jpg

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J Matern Fetal Neonatal Med. 2022 Dec;35(25):8012-8018. doi: 10.1080/14767058.2021.1940935. Epub 2021 Jun 28.
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Conflicting Nongenomic Effects of Progesterone in the Myometrium of Pregnant Rats.孕激素在妊娠大鼠子宫中的非基因组冲突效应。
Int J Mol Sci. 2021 Feb 22;22(4):2154. doi: 10.3390/ijms22042154.
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Progestins Inhibit Interleukin-1β-Induced Matrix Metalloproteinase 1 and Interleukin 8 Expression via the Glucocorticoid Receptor in Primary Human Amnion Mesenchymal Cells.
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Front Immunol. 2024 Dec 19;15:1470283. doi: 10.3389/fimmu.2024.1470283. eCollection 2024.
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Heliyon. 2024 Mar 24;10(7):e28483. doi: 10.1016/j.heliyon.2024.e28483. eCollection 2024 Apr 15.
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Evaluation of the antibacterial activity of essential oil against halitosis-related and .评估香精油对与口臭相关的……的抗菌活性。 (原文此处不完整)
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