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(ICAM\u20101) production of endothelial cells, which are crucial to angiogenesis and pulpal\/periapical wound healing.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methodology<\/jats:title><jats:p>Endothelial cells were exposed to butyrate with\/without inhibitors. Cell viability, apoptosis and reactive oxygen species (ROS) were evaluated using an MTT assay, PI\/annexin V and DCF fluorescence flow cytometry respectively. RNA and protein expression was determined using a polymerase chain reaction assay and Western blotting or immunofluorescent staining. Soluble ICAM\u20101 (sICAM\u20101) was measured using an enzyme\u2010linked immunosorbent assay. The quantitative results were expressed as mean\u00a0\u00b1\u00a0standard error (SE) of the mean. The data were analysed using a paired Student's <jats:italic>t<\/jats:italic>\u2010test where necessary. A <jats:italic>p<\/jats:italic>\u2010value \u22640.05 was considered to indicate a statistically significant difference between groups.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Butyrate (&gt;4\u00a0mM) inhibited cell viability and induced cellular apoptosis and necrosis. It inhibited cyclin B1 but stimulated p21 and p27 expression. Butyrate stimulated ROS production and hemeoxygenase\u20101 (HO\u20101) expression as well as activated the Ac\u2010H3, p\u2010ATM, p\u2010ATR, p\u2010Chk1, p\u2010Chk2, p\u2010p38 and p\u2010Akt expression of endothelial cells. Butyrate stimulated ICAM\u20101\u00a0mRNA\/protein expression and significant sICAM\u20101 production (<jats:italic>p<\/jats:italic>\u00a0&lt;\u00a0.05). Superoxide dismutase, 5z\u20107oxozeaenol, SB203580 and compound C (<jats:italic>p<\/jats:italic>\u00a0&lt;\u00a0\u00a0.05), but not ZnPP, CGK733, AZD7762 or LY294002, attenuated butyrate cytotoxicity to endothelial cells. Notably, little effect on butyrate\u2010stimulated sICAM\u20101\u00a0secretion was found. Valproic acid, phenylbutyrate and trichostatin (three histone deacetylase inhibitors) significantly induced sICAM\u20101 production (<jats:italic>p<\/jats:italic>\u00a0&lt;\u00a0.05).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Butyric acid inhibited proliferation, induced apoptosis, stimulated ROS and HO\u20101 production and increased ICAM\u20101\u00a0mRNA expression and protein synthesis in endothelial cells. Cell viability affected by BA was diminished by some inhibitors; however, the increased sICAM\u20101\u00a0secretion by BA was not affected by any of the tested inhibitors. These results facilitate understanding of the pathogenesis, prevention and treatment of pulpal\/periapical diseases.<\/jats:p><\/jats:sec>","DOI":"10.1111\/iej.13614","type":"journal-article","created":{"date-parts":[[2021,8,22]],"date-time":"2021-08-22T09:44:53Z","timestamp":1629625493000},"page":"38-53","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Effect of butyrate, a bacterial by\u2010product, on the viability and ICAM\u20101 expression\/production of human vascular endothelial cells: Role in infectious pulpal\/periapical diseases"],"prefix":"10.1111","volume":"55","author":[{"given":"Mei\u2010Chi","family":"Chang","sequence":"first","affiliation":[{"name":"Chang Gung University of Science and Technology Taoyuan City Taiwan"},{"name":"Department of Dentistry Chang Gung Memorial Hospital Taipei 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