The protective effect of vitexinin septic encephalopathy by reducing leukocyte-endothelial adhesion and inflammatory response.

Annals of Palliative Medicine
Haiquan CaoMeiping Ren

Abstract

Despite advances in therapeutic strategies and critical care management, septic encephalopathy (SE) is still a leading cause of infection-associated death in intensive care units (ICUs). Vitexin, a flavonoids compound, exerts and anti-inflammatory effect through inhibition of proinflammatory cytokines and signaling pathways. This study aimed to explore the anti-inflammatory effects of vitexin in SE and the underlying mechanisms. An SE-inducedC57BL/6 mouse model was established via cecal ligation and puncture (CLP). Western blotting was performed to evaluate the protein expression levels of Chemokine (C-X-C motif) ligand 1 (CXCL1), fractalkine (CX3CL1), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, NF-κB p65, p-NF-κB p65, and tumor necrosis factor-α (TNF-α). Flow cytometry was used to detect the expressions ofCD11a/CD18, CD11b/CD18, ICAM-1, and adherent leukocyte. The expression of ICAM-1 was detected by immunohistochemistry. An enzyme-linked immunosorbent assay was performed to evaluate the expression of monocyte chemotactic protein-1 (MCP-1), Interleukin (IL)-6, IL-8, and IL-10. In this study, we found that vitexin significantly downregulated the expression of brain endothe...Continue Reading

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