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Lipopolysaccharide promotes the development of murine endometriosis‐like lesions via the nuclear factor‐kappa B pathway
Author(s) -
Azuma Yukihiro,
Taniguchi Fuminori,
Nakamura Kazuomi,
Nagira Kei,
Khine Yin Mon,
Kiyama Tomoiki,
Uegaki Takashi,
Izawa Masao,
Harada Tasuku
Publication year - 2017
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12631
Subject(s) - endometriosis , lipopolysaccharide , inflammation , immunohistochemistry , medicine , nf κb , nfkb1 , andrology , cancer research , chemistry , transcription factor , gene , biochemistry
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 CD 3, 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.

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