Salidroside regulates the expressions of IL-6 and defensins in LPS-activated intestinal epithelial cells through NF-κB/MAPK and STAT3 pathways
Authors
Abstract:
Objective(s): To reveal the detailed mechanism underlying the functions of salidroside on the inflammation of intestinal epithelial cells during IBD.Materials and Methods: Quantitative real-time PCR was employed to assess the expression of IL-6, IL-10, and α-defensins 5 and 6. ELISA assay was performed to measure the secretion of IL-6 and IL-10. MTT assay was used to determine the cell viability and proliferation. Western blot was used to assess the phosphorylation of NF-kB, Erk1/2, JNK, P38, JAK2, and STAT3. Results: Salidroside impaired the proliferation of intestinal epithelial cells at high concentrations (P< 0.05) and down-regulated interleukin-6 (IL-6) production induced by LPS (P
similar resources
Bcl10 mediates LPS-induced activation of NF-kappaB and IL-8 in human intestinal epithelial cells.
Lipopolysaccharide (LPS) is recognized as an inducer of the inflammatory response associated with gram-negative sepsis and systemic inflammatory response syndrome. LPS induction proceeds through Toll-like receptor (TLR) in immune cells and intestinal epithelial cells (IEC). This report presents the first identification of Bcl10 (B-cell CLL/lymphoma 10) as a mediator of the LPS-induced activatio...
full textBcl10 mediates LPS-induced activation of NF- B and IL-8 in human intestinal epithelial cells
Bhattacharyya S, Borthakur A, Pant N, Dudeja PK, Tobacman JK. Bcl10 mediates LPS-induced activation of NFB and IL-8 in human intestinal epithelial cells. Am J Physiol Gastrointest Liver Physiol 293: G429–G437, 2007. First published May 31, 2007; doi:10.1152/ajpgi.00149.2007.—Lipopolysaccharide (LPS) is recognized as an inducer of the inflammatory response associated with gram-negative sepsis an...
full textITF promotes migration of intestinal epithelial cells through crosstalk between the ERK and JAK/STAT3 pathways
Intestinal trefoil factor (ITF), a member of the trefoil factor family, is a "Super-protective factor" for intestinal mucosal protection. This study was designed to explore the mechanism by which ITF promotes intestinal epithelial cell migration. Intestinal epithelial cells were treated with the human ITF (hITF). Phospho-ERK, phospho-STAT3 Tyr(705), and phospho-STAT3 Ser(727) levels were detect...
full textRhoE/ROCK2 regulates chemoresistance through NF-κB/IL-6/ STAT3 signaling in hepatocellular carcinoma
Small Rho GTPase (Rho) and its immediate effector Rho kinase (ROCK) are reported to regulate cell survival, but the detailed molecular mechanism remains largely unknown. We had previously shown that Rho/ROCK signaling was highly activated in hepatocellular carcinoma (HCC). In this study, we further demonstrated that downregulation of RhoE, a RhoA antagonist, and upregulation of ROCK enhanced re...
full textDetection of IL-20R1 and IL-20R2 mRNA in C57BL/6 Mice Astroglial Cells and Brain Cortex Following LPS Stimulation
Background: Astrocytes, which comprise ~90% of overall brain mass, are involved in brain immunity. These cells represent the non-professional class of CNS-resident APCs and may promote or inhibit CNS inflammation depending on the cytokines they secrete. IL-10 family of cytokines and their receptors, IL-20R1 and IL-20R2, may have a role in shifting astrocytes to a neuroprotective or neurodegener...
full textstudy of the expressions of il-20r1 and il-20r2 in c57bl/6 mice astroglial cells
objective: astrocytes are the most abundant glial cell type. they may promote or inhibit cns inflammation depending on which cytokines are secreted. astrocytes also have immune roles. il-19, il-20, and il-24 activate a heterodimer receptor composed of the il-20r1 α-chain and the il-20r2 β-chain. it has long been considered that signaling by these receptor complexes affects immunological reactio...
full textMy Resources
Journal title
volume 22 issue 1
pages 31- 37
publication date 2019-01-01
By following a journal you will be notified via email when a new issue of this journal is published.
Hosted on Doprax cloud platform doprax.com
copyright © 2015-2023