The protective effect of vitexinin septic encephalopathy by reducing leukocyte-endothelial adhesion and inflammatory response
| Autor: | Haiquan Cao, Bing Zhang, Meiping Ren, Xiaojuan Wang |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Chemokine Vitexin Vascular Cell Adhesion Molecule-1 CD18 Pharmacology Proinflammatory cytokine 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine Intensive care Cell Adhesion Leukocytes Medicine Animals Endothelium Apigenin CX3CL1 Cell adhesion Advanced and Specialized Nursing Inflammation Brain Diseases biology Cell adhesion molecule business.industry Tumor Necrosis Factor-alpha Intercellular Adhesion Molecule-1 030104 developmental biology Anesthesiology and Pain Medicine chemistry 030220 oncology & carcinogenesis biology.protein business |
| Zdroj: | Annals of palliative medicine. 9(4) |
| ISSN: | 2224-5839 |
| Popis: | Background 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. Methods 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. Results In this study, we found that vitexin significantly downregulated the expression of brain endothelial chemokines CXCL1 and CX3CL1 in CLP mice, exerting a potential anti-inflammatory against SE. Our data also showed that vitexin alleviated SE primarily by relying on reducing leukocyte-endothelial adhesion via the mediation of adhesion molecules. Moreover, vitexin suppressed the expression of proinflammatory cytokines, such as MCP-1, IL-6, IL-8, TNF-α, and NF-κB p65, in the CLP mice, while the expression of the anti-inflammatory cytokine IL-10 was elevated. Conclusions Overall, our study demonstrated the protective effect vitexin exerts in SE by reducing leukocyte-endothelial adhesion and inflammatory response. These findings offer a molecular basis for the potential application of vitexin in the treatment of SE and other inflammatory-mediated and immunemediated disorders. |
| Databáze: | OpenAIRE |
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