{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,4]],"date-time":"2026-11-04T20:52:49Z","timestamp":1793825569194,"version":"4.6.1"},"reference-count":69,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,2,11]],"date-time":"2026-02-11T00:00:00Z","timestamp":1770768000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    Inflammation and endothelial dysfunction are key steps in the pathogenesis of atherosclerosis. Octacosanol (C\n                    <jats:sub>28<\/jats:sub>\n                    H\n                    <jats:sub>58<\/jats:sub>\n                    O, OCT), a very-long-chain saturated aliphatic alcohol (VLCA) with 28 carbons, is the main component of policosanol, a nutraceutical mixture of VLCAs (C20-C34) extracted from plants. Polycosanol in animal models is known to reduce atherosclerosis, but its mechanism of action remains unclear. This study investigates the pathways by which OCT alleviates LPS-induced inflammation in primary human aortic endothelial cells (HAECs). After overnight pretreatment with purified OCT, inflammation in HAECs was induced by lipopolysaccharide (LPS) at 100 ng\/ml. The effects of OCT on the levels of pro-inflammatory cytokines, and molecules involved in inflammation signaling pathway, cell adhesion, and cell integrity were examined using quantitative RT-PCR, enzyme-linked immunosorbent assay, flow cytometry, or confocal microscopy in LPS-stimulated HAECs. The group of untreated HAECs was used as a control. OCT pretreatment of HAECs significantly reduced LPS-induced inflammatory responses, decreasing levels of IL-6, IL-8, and MCP-1 mRNA and protein, as well as TLR4, MYD88, TIRAP, TRAF6, and IRAK1 mRNA (p &amp;lt; 0.05). In a monocyte adhesion assay, LPS exposure increased human monocytic cells (THP-1) adherence to HAECs, whereas OCT pretreatment suppressed the LPS-induced adhesion of THP-1 to HAECs in a time- and dose-dependent manner, by blocking the mRNA and protein expression of adhesion molecules (VCAM-1, ICAM-1, P- and E-SELECTIN) (p &amp;lt; 0.05). OCT also suppressed mRNA and protein levels of CORTACTIN, VINCULIN, and TALIN, and inhibited focal adhesion and lamellipodia formation, cell deformation, and migration in response to LPS (p &amp;lt; 0.05). In addition, an endothelial permeability assay revealed that OCT pretreatment also improved endothelial cell integrity after LPS stimulation by preserving both adherens junctions and tight junctions formed by VE-CADHERIN, \u03b2 -CATENIN, and Zonula Occludens-1 (ZO-1) (p &amp;lt; 0.05). In summary, the multiple cytoprotective effects of OCT against LPS-induced inflammation in endothelial cells could contribute to the anti-atherogenic properties of policosanol.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2026.1770191","type":"journal-article","created":{"date-parts":[[2026,2,11]],"date-time":"2026-02-11T07:41:49Z","timestamp":1770795709000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":3,"title":["Cytoprotective role of octacosanol in lipopolysaccharide-induced inflammation"],"prefix":"10.3389","volume":"17","author":[{"given":"Jingrong","family":"Tang","sequence":"first","affiliation":[{"name":"Lipoprotein Metabolism Laboratory, National Heart, Lung and Blood Institute (NHLBI), National Institutes of Health (NIH)","place":["Bethesda, MD, United 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