脂多糖通过核因子-κB途径促进小鼠子宫内膜异位症样病变的发展。

Lipopolysaccharide promotes the development of murine endometriosis-like lesions via the nuclear factor-kappa B pathway.

作者信息

Azuma Yukihiro, Taniguchi Fuminori, Nakamura Kazuomi, Nagira Kei, Khine Yin Mon, Kiyama Tomoiki, Uegaki Takashi, Izawa Masao, Harada Tasuku

机构信息

Department of Obstetrics and Gynecology, Tottori University Faculty of Medicine, Yonago, Japan.

Division of Laboratory Animal Science, Research Center for Bioscience and Technology, Tottori University Faculty of Medicine, Yonago, Japan.

出版信息

Am J Reprod Immunol. 2017 Apr;77(4). doi: 10.1111/aji.12631. Epub 2017 Jan 31.

DOI:10.1111/aji.12631

PMID:28138997

Abstract

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.

摘要

问题

脂多糖（LPS）是否参与子宫内膜异位症的发生发展？

研究方法

将69只BALB/c小鼠用于建立小鼠子宫内膜异位症模型。对手术诱导的子宫内膜异位症小鼠进行腹腔注射LPS。在注射LPS 4周后，无论是否使用核因子-κB（NF-κB）抑制剂，评估子宫内膜异位样病变的程度。使用实时逆转录聚合酶链反应（RT-PCR）评估植入物中炎症因子的表达。通过免疫组织化学染色评估细胞增殖、血管生成活性、炎症和NF-κB磷酸化。

结果

脂多糖增加了子宫内膜异位样病变中Ptgs-2、Vegf、Ccl-2和Il-6的总数、大小及mRNA表达。LPS还增加了Ki67阳性细胞的百分比，并增强了CD3、F4/80和PECAM阳性细胞的强度和比例。观察到LPS给药后磷酸化NF-κB p65的强烈表达。用NF-κB抑制剂治疗可消除这些LPS诱导的效应。