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Updated: Mar 8, 2026
A Syngeneic Murine Model of Endometriosis using Naturally Cycling Mice
Published on: November 24, 2020
Lipopolysaccharide promotes the development of murine endometriosis-like lesions via the nuclear factor-kappa B
Yukihiro Azuma1, Fuminori Taniguchi1, Kazuomi Nakamura2
1Department of Obstetrics and Gynecology, Tottori University Faculty of Medicine, Yonago, Japan.
Problem:
Is lipopolysaccharide (LPS) involved in the development of endometriosis?
Method Of Study:
BALB/c mice (n=69) were used for the murine endometriosis model. Mice with surgically induced endometriosis were injected with LPS intraperitoneally. After 4 weeks of LPS injections with or without the nuclear factor-kappa B (NF-κB) inhibitor, the extent of endometriosis-like lesions was evaluated. Expression of inflammatory factors in the implants was evaluated using real-time RT-PCR. Cell proliferation, angiogenic activity, inflammation, and NF-κB phosphorylation were assessed by immunohistochemical staining.
Results:
Lipopolysaccharide increased total number, size, and mRNA expression of Ptgs-2, Vegf, Ccl-2, and Il-6 in endometriosis-like lesions. LPS also increased the percentage of Ki67-positive cells and enhanced the intensity and rate of positive cells of CD3, F4/80, and PECAM. Intense expression of phospho-NF-κB p65 after LPS administration was observed. Treatment with the NF-kB inhibitor negated these LPS-induced effects.
Conclusion:
LPS-induced pelvic inflammation status enhanced the development of murine endometriosis-like lesions via NF-κB pathway.
