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[DOI] [PubMed] [Google Scholar] Bardania, H
سيروم هيالورونيك وجلوتاثيون
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These molecular events collectively increase blood-brain barrier (BBB) paracellular permeability, thereby permitting passive diffusion of peripheral inflammatory mediators and autoantibodies into the central nervous system (CNS) ( In vitro studies have demonstrated that combined treatment with TNF-α and IFN-γ significantly reduces transendothelial electrical resistance in brain endothelial cells and induces redistribution of occludin and ZO-1 from intercellular junctions to the cytoplasm ( Second, the transcellular active transport pathway: IL-17 and IL-22 act directly on cerebrovascular endothelial cells expressing their cognate receptors, disrupting tight junction integrity and upregulating expression of adhesion molecules (ICAM-1 and VCAM-1) on the endothelial cell surface, thereby facilitating Th17 cell transmigration across the BBB ( 1.1 Experimental approaches to test the hypothesis This hypothesis could be experimentally tested through the following approaches: (i) analysis of correlations between peripheral blood cytokine profiles (IFN-γ, IL-17, IL-6, and TNF-α) and cerebrospinal fluid (CSF) inflammatory markers (such as CXCL13 and neurofilament light chain [NfL]) in MG patients
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