Frontiers in Pharmacology
Benzyl isothiocyanate alleviates neural damage in experimental autoimmune uveitis by modulating the TREM-1/PI3K/AKT signaling pathway
By Sijie Liu, Wendan Yi, Yiqing Ji and 7 others.
Abstract
Purpose
To investigate whether Benzyl isothiocyanate (BITC) can improve experimental autoimmune uveitis (EAU) and explore its potential mechanism.
Methods
To evaluate the therapeutic efficacy of BITC, EAU was induced in C57BL/6 mice via immunization with IRBP 651-670 . 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. In vitro , BV2 cells were exposed to lipopolysaccharide (LPS) and interferon-γ (IFN-γ). 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).
