{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T06:04:21Z","timestamp":1790229861754,"version":"4.1.0"},"reference-count":67,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T00:00:00Z","timestamp":1790208000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82274585"],"award-info":[{"award-number":["82274585"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Pharmacol."],"abstract":"<jats:p>\n                    <jats:bold>Purpose:<\/jats:bold>\n                    To investigate whether Benzyl isothiocyanate (BITC) can improve experimental autoimmune uveitis (EAU) and explore its potential mechanism.\n                    <jats:bold>Methods:<\/jats:bold>\n                    To evaluate the therapeutic efficacy of BITC, EAU was induced in C57BL\/6 mice\n                    <jats:italic>via<\/jats:italic>\n                    immunization with IRBP\n                    <jats:sub>651-670<\/jats:sub>\n                    . Clinical scores and histopathological staining were employed to evaluate the severity of the disease. The integrity of the blood-retinal barrier (BRB) was assessed using Evans blue staining and Western blot analysis. Nissl staining, Brn3a immunofluorescence, and TUNEL assay were employed to assess retinal neuronal damage.\n                    <jats:italic>In vitro<\/jats:italic>\n                    , BV2 cells were exposed to lipopolysaccharide (LPS) and interferon-\u03b3 (IFN-\u03b3). Biochemical markers of oxidative stress, mRNA levels of phagocytosis-related markers, protein and mRNA levels of neurotrophic factors, and triggering receptor expressed on myeloid cells-1 (TREM-1) were measured. Additionally, conditioned medium from BV2 cells was co-cultured with primary retinal ganglion cells (RGCs) to detect apoptosis. The functional relevance of TREM-1 in the protective effects of BITC was evaluated by overexpressing TREM-1 (oe-TREM-1).\n                    <jats:bold>Results:<\/jats:bold>\n                    In vivo, BITC alleviated clinical symptoms of EAU mice. Treatment significantly maintained BRB integrity and mitigated oxidative stress and neuronal damage.\n                    <jats:italic>In vitro<\/jats:italic>\n                    , BITC suppressed oxidative stress and phagocytic activity. The co-culture study of BV2 cells and primary RGCs showed that BITC can alleviate LPS + IFN-\u03b3 induced primary RGCs damage and inhibit apoptosis. Furthermore, BITC downregulated the expression of TREM-1\/PI3K\/AKT signaling pathway in EAU mice and LPS + IFN-\u03b3 induced BV2 cells. Oe-TREM-1 partially eliminated the inhibitory effects of BITC on oxidative stress and phagocytosis, as well as its protective effect against neuronal damage.\n                    <jats:bold>Conclusion:<\/jats:bold>\n                    BITC alleviates neural damage in EAU by down-regulating the TREM-1\/PI3K\/AKT signaling pathway, reducing oxidative stress and excessive phagocytosis, and promoting the secretion of neurotrophic factors.\n                  <\/jats:p>","DOI":"10.3389\/fphar.2026.1948992","type":"journal-article","created":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T05:43:25Z","timestamp":1790228605000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Benzyl isothiocyanate alleviates neural damage in experimental autoimmune uveitis by modulating the TREM-1\/PI3K\/AKT signaling 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