Inhibition of LPS-induced inflammation and signaling pathways in fallopian tube epithelial cells by estrogen and progesterone

Abstract Aim The inhibitory effects of estrogen and progesterone on lipopolysaccharide (LPS)-induced inflammation and the nuclear factor-κB (NF-κB), mitogen-activated protein kinase (MAPK), and phosphoinositide-3 kinase (PI3K)/protein kinase B (Akt) signaling pathways in mouse oviductal epithelial c...

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Main Authors: Qianqian Li, Jianqi Liu, Bayaer Nashun, Sarina Bai, Xiaozhen Guo, Ling Wu, Tuya Bao
Format: Article
Language:English
Published: BMC 2025-07-01
Series:BMC Veterinary Research
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Online Access:https://doi.org/10.1186/s12917-025-04874-x
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author Qianqian Li
Jianqi Liu
Bayaer Nashun
Sarina Bai
Xiaozhen Guo
Ling Wu
Tuya Bao
author_facet Qianqian Li
Jianqi Liu
Bayaer Nashun
Sarina Bai
Xiaozhen Guo
Ling Wu
Tuya Bao
author_sort Qianqian Li
collection DOAJ
description Abstract Aim The inhibitory effects of estrogen and progesterone on lipopolysaccharide (LPS)-induced inflammation and the nuclear factor-κB (NF-κB), mitogen-activated protein kinase (MAPK), and phosphoinositide-3 kinase (PI3K)/protein kinase B (Akt) signaling pathways in mouse oviductal epithelial cells were investigated. Methods Mouse oviduct epithelial cells were isolated for various in vitro experiments. The CCK-8 method was used to detect the effects of LPS, LPS + Dexamethasone (DXM), LPS + E2, and LPS + P4 on the viability of fallopian tube epithelial cells. RT‒qPCR was used to measure the expression levels of IL-1β, TNF-α, IL-10, and β-defensin-2 (mBD-2) in cells. ELISA was used to measure the levels of IL-1β in cells. Western blotting was used to detect the protein expression of NF-κB p65, IκBα, p38, P-p38, Akt, and P-Akt in cells. Additionally, a salpingitis mouse model was constructed with LPS, and the model mice were treated with estrogen (E2), progesterone (P4), and DXM. The ovarian tissues were collected and subjected to HE staining. Moreover, IL-10 and mBD-2 expression in the tissue was detected by immunohistochemical staining. Key findings Estrogen and progesterone significantly inhibited the production of IL-1β, TNF-α, IL-10, and mBD-2, thereby effectively suppressing the inflammatory response induced by LPS. In terms of signaling pathways, estrogen and progesterone significantly inhibited the protein expression of NF-κB, MAPK, and PI3K/Akt pathway members induced by LPS. Significance Estrogen and progesterone can protect against LPS-induced mouse salpingitis by inhibiting the activation of the NF-κB, MAPK, and PI3K/Akt signaling pathways and suppressing the expression of the inflammatory factors IL-1β, TNF-α, IL-10, and mBD-2. Brief Summary Estrogen and progesterone can effectively reduce the inflammatory response of the fallopian tubes. Strengths and limitations of this study The advantages of this study are as follows: high data reliability; a large number of experimental repetitions, resulting in stable outcomes; and a concise and efficient explanation of the issues. Limitation The research objective is too broad.
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institution Kabale University
issn 1746-6148
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series BMC Veterinary Research
spelling doaj-art-3eaf205237db4708a85e13324268f3212025-08-20T03:45:32ZengBMCBMC Veterinary Research1746-61482025-07-0121111210.1186/s12917-025-04874-xInhibition of LPS-induced inflammation and signaling pathways in fallopian tube epithelial cells by estrogen and progesteroneQianqian Li0Jianqi Liu1Bayaer Nashun2Sarina Bai3Xiaozhen Guo4Ling Wu5Tuya Bao6School of Basic Medicine, Inner Mongolia Medical UniversitySchool of Basic Medicine, Inner Mongolia Medical UniversitySchool of Basic Medicine, Inner Mongolia Medical UniversitySchool of Basic Medicine, Inner Mongolia Medical UniversitySchool of Basic Medicine, Inner Mongolia Medical UniversitySchool of Basic Medicine, Inner Mongolia Medical UniversitySchool of Basic Medicine, Inner Mongolia Medical UniversityAbstract Aim The inhibitory effects of estrogen and progesterone on lipopolysaccharide (LPS)-induced inflammation and the nuclear factor-κB (NF-κB), mitogen-activated protein kinase (MAPK), and phosphoinositide-3 kinase (PI3K)/protein kinase B (Akt) signaling pathways in mouse oviductal epithelial cells were investigated. Methods Mouse oviduct epithelial cells were isolated for various in vitro experiments. The CCK-8 method was used to detect the effects of LPS, LPS + Dexamethasone (DXM), LPS + E2, and LPS + P4 on the viability of fallopian tube epithelial cells. RT‒qPCR was used to measure the expression levels of IL-1β, TNF-α, IL-10, and β-defensin-2 (mBD-2) in cells. ELISA was used to measure the levels of IL-1β in cells. Western blotting was used to detect the protein expression of NF-κB p65, IκBα, p38, P-p38, Akt, and P-Akt in cells. Additionally, a salpingitis mouse model was constructed with LPS, and the model mice were treated with estrogen (E2), progesterone (P4), and DXM. The ovarian tissues were collected and subjected to HE staining. Moreover, IL-10 and mBD-2 expression in the tissue was detected by immunohistochemical staining. Key findings Estrogen and progesterone significantly inhibited the production of IL-1β, TNF-α, IL-10, and mBD-2, thereby effectively suppressing the inflammatory response induced by LPS. In terms of signaling pathways, estrogen and progesterone significantly inhibited the protein expression of NF-κB, MAPK, and PI3K/Akt pathway members induced by LPS. Significance Estrogen and progesterone can protect against LPS-induced mouse salpingitis by inhibiting the activation of the NF-κB, MAPK, and PI3K/Akt signaling pathways and suppressing the expression of the inflammatory factors IL-1β, TNF-α, IL-10, and mBD-2. Brief Summary Estrogen and progesterone can effectively reduce the inflammatory response of the fallopian tubes. Strengths and limitations of this study The advantages of this study are as follows: high data reliability; a large number of experimental repetitions, resulting in stable outcomes; and a concise and efficient explanation of the issues. Limitation The research objective is too broad.https://doi.org/10.1186/s12917-025-04874-xEstrogenProgesteroneLPSNF-κBMAPKPI3K/Akt
spellingShingle Qianqian Li
Jianqi Liu
Bayaer Nashun
Sarina Bai
Xiaozhen Guo
Ling Wu
Tuya Bao
Inhibition of LPS-induced inflammation and signaling pathways in fallopian tube epithelial cells by estrogen and progesterone
BMC Veterinary Research
Estrogen
Progesterone
LPS
NF-κB
MAPK
PI3K/Akt
title Inhibition of LPS-induced inflammation and signaling pathways in fallopian tube epithelial cells by estrogen and progesterone
title_full Inhibition of LPS-induced inflammation and signaling pathways in fallopian tube epithelial cells by estrogen and progesterone
title_fullStr Inhibition of LPS-induced inflammation and signaling pathways in fallopian tube epithelial cells by estrogen and progesterone
title_full_unstemmed Inhibition of LPS-induced inflammation and signaling pathways in fallopian tube epithelial cells by estrogen and progesterone
title_short Inhibition of LPS-induced inflammation and signaling pathways in fallopian tube epithelial cells by estrogen and progesterone
title_sort inhibition of lps induced inflammation and signaling pathways in fallopian tube epithelial cells by estrogen and progesterone
topic Estrogen
Progesterone
LPS
NF-κB
MAPK
PI3K/Akt
url https://doi.org/10.1186/s12917-025-04874-x
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