The Mechanism of Notopterol Alleviating LPS-induced Endometritis  by Inhibiting the TLR4/NF-κB Signaling Pathway

Zhaomei  Xu; Yanan  Zhang; Jinfeng  Pang; Xiao  Chen; Yulong  Chen; Yafei  Chen; Yingwei  Wang

doi:10.18502/ijaai.v24i6.20162

Zhaomei Xu Clinical Laboratory, Tiantai People’s Hospital, Zhejiang, China
Yanan Zhang Clinical Laboratory, Tiantai People’s Hospital, Zhejiang, China
Jinfeng Pang Department of Gynecology and Obstetrics, Tiantai People’s Hospital, Zhejiang, China
Xiao Chen Clinical Laboratory, Tiantai People’s Hospital, Zhejiang, China
Yulong Chen Clinical Laboratory, Tiantai People’s Hospital, Zhejiang, China
Yafei Chen Clinical Laboratory, Tiantai People’s Hospital, Zhejiang, China
Yingwei Wang Clinical Laboratory, Tiantai People’s Hospital, Zhejiang, China

DOI: https://doi.org/10.18502/ijaai.v24i6.20162

Keywords: Endometritis; Inflammation; Lipopolysaccharide; Notopterol

Abstract

This study aims to investigate the role of notopterol in alleviating endometritis induced by lipopolysaccharide (LPS) and to explore its underlying mechanisms.Human endometrial epithelial cells (hEECs) were treated with LPS to establish an in vitro model of endometritis, and the cells were divided into five groups: control, LPS, LPS+notopterol(15 mol/L), LPS+notopterol(305 mol/L) and LPS+notopterol(45 mol/L) groups. The expression levels of inflammatory factors were determined by Enzyme-Linked ImmunoSorbent Assay (ELISA). Apoptosis was detected by TdT-mediated dUTP Nick-End Labeling (TUNEL) method. Cell viability was determined by Cell Counting Kit-8 (CCK-8) test. Western blot was used to detect the expression levels of nuclear factor κB(NF-κB) p65, NF-κB inhibitor (IκBα), p-NF-κB p65 and p-IκBα.

Following LPS treatment, cytokine levels significantly increased compared to the control group.; moreover, cell proliferation decreased, apoptosis increased, and the expression level of p-NF-κB p65 was increased. Subsequently, the LPS-treated hEECs were exposed to notopterygium. Compared to the LPS group.

Treatment with LPS + notopterol resulted in a dose-dependent reduction in inflammatory cytokines, increased cell proliferation, and a significant reduction in apoptosis. Furthermore, the expression levels of p-NF-κB p65 and p-IκBα were downregulated.

These findings suggest that notopterol alleviates LPS-induced endometritis by inhibiting the TLR4/NF-κB signaling pathway.