Li-Bing Liu

No ORCID on file · 9 papers in corpus · active 2013-2022

Study types

  • article 9

Condition tags

  • mesh:D004715 9
  • endometriosis 9
article 2022
Ornidazole Reduces the Progression of Endometriosis in a Rat Model
Gynecologic and obstetric investigation ·doi:10.1159/000527515

Objective: The aim of this study was to investigate the effectiveness of ornidazole in inhibiting the progression of endometriosis in a rat model. Design: This was an in vivo experiment, including the ornidazole group (n = 16) and a control…

article 2019
IL-2 and IL-27 synergistically promote growth and invasion of endometriotic stromal cells by maintaining the balance of IFN-γ and IL-10 in endometriosis
Reproduction (Cambridge, England) ·doi:10.1530/rep-19-0411

Immune cells and cytokines have important roles in the pathogenesis of endometriosis. However, the production and role of cytokines of T helper type 1 (Th1) and Th2 cells in the progress of endometriosis have remained to be fully elucidated…

article 2018
Estrogen restricts the apoptosis of endometrial stromal cells by promoting TSLP secretion
Molecular medicine reports ·doi:10.3892/mmr.2018.9428

Endometriosis (EMS) is a female hormone‑ dependent disease with controversial reports of its etiology and pathogenesis. Apoptosis is particularly important in the human endometrium due to the dynamic cycles of proliferation and shedding. Es…

article 2018
Indoleamine 2,3-dioxygenase suppresses the cytotoxicity of NK cells in response to ectopic endometrial stromal cells in endometriosis
Reproduction (Cambridge, England) ·doi:10.1530/rep-18-0112

It has been reported that the impaired cytotoxicity of natural killer (NK) cells and abnormal cytokines that are changed by the interaction between ectopic endometrial cells and immune cells is indispensable for the initiation and developme…

article 2017
IL-27 triggers IL-10 production in Th17 cells via a c-Maf/RORγt/Blimp-1 signal to promote the progression of endometriosis
Cell death & disease ·doi:10.1038/cddis.2017.95

Abstract Endometriosis is an estrogen-dependent inflammatory disease. The anti-inflammatory cytokine IL-10 is also increased in endometriosis. IL-10 production by Th17 cells is critical for limiting autoimmunity and inflammatory responses. …

article 2016
IL15 promotes growth and invasion of endometrial stromal cells and inhibits killing activity of NK cells in endometriosis
Reproduction (Cambridge, England) ·doi:10.1530/rep-16-0089

Endometriosis (EMS) is associated with an abnormal immune response to endometrial cells, which can facilitate the implantation and proliferation of ectopic endometrial tissues. It has been reported that human endometrial stromal cells (ESCs…

article 2014
TSLP induced by estrogen stimulates secretion of MCP-1 and IL-8 and growth of human endometrial stromal cells through JNK and NF-κB signal pathways.
International journal of clinical and experimental pathology

It has reported that human endometrial stromal cells (ESCs) express thymic stromal lymphopoietin (TSLP), and TSLP concentrations in the serum and peritoneal fluid were higher in women with endometriosis. Endometriosis is an estrogen-depende…

article 2013
IL-22 in the endometriotic milieu promotes the proliferation of endometrial stromal cells via stimulating the secretion of CCL2 and IL-8.
International journal of clinical and experimental pathology

Interleukin-22 (IL-22) is a member of the IL-10 cytokine family and plays critical roles in inflammation, immune surveillance, and tissue homeostasis. However, whether IL-22 regulates the growth of endometrial stromal cells (ESCs), and part…

article 2013
NME1 suppression of endometrial stromal cells promotes angiogenesis in the endometriotic milieu via stimulating the secretion of IL-8 and VEGF.
International journal of clinical and experimental pathology

Nonmetastatic gene 23-H1 (NME1, also known as nm23-H1) is a wide-spectrum tumor metastasis suppressor gene that plays an important role in suppressing the proliferation, adhesion and invasion of endometrial stromal cells (ESCs). The present…