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Recent reports indicate OX plays an important role in the progression of inflammatory diseases such as rheumatoid arthritis. Pulpitis is caused by the activation of the biological defense mechanism of the dental pulp against cariogenic bacteria. However, the role of OX in the pathogenesis of pulpitis remains unknown. The aim of this study was to examine the effect of OX on CXC chemokine ligand 10 (CXCL10) production in human dental pulp stem cells (HDPSCs). Expression of the oxytocin receptor (OXR) on HDPSCs was detected by Western blot analysis and immunofluorescence. CXCL10 production in HDPSCs was measured using an enzyme\u2010linked immunosorbent assay kit. Western blot analysis was performed to determine the phosphorylation levels of signal transduction molecules, including nuclear factor kappa B, mitogen\u2010activated protein kinases (MAPKs), and Akt in HDPSCs. HDPSCs expressed OXR. OX significantly decreased CXCL10 production in tumor necrosis factor (TNF)\u2010\u03b1\u2010stimulated HDPSCs. The p38 MAPK and Akt pathways were related to the OX\u2010suppressed CXCL10 production in TNF\u2010\u03b1\u2010stimulated HDPSCs. These results indicate that OX appears to modulate the immune response in pulpitis via suppression of CXCL10 production by HDPSCs.<\/jats:p>","DOI":"10.1002\/cbin.11860","type":"journal-article","created":{"date-parts":[[2022,7,23]],"date-time":"2022-07-23T18:57:50Z","timestamp":1658602670000},"page":"1530-1535","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Oxytocin suppresses CXCL10 production in TNF\u2010\u03b1\u2010stimulated human dental pulp stem cells"],"prefix":"10.1002","volume":"46","author":[{"given":"Tomoki","family":"Kumagai","sequence":"first","affiliation":[{"name":"Department of Biological Endodontics, Graduate School of Biomedical and Health Sciences Hiroshima University Hiroshima 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