CXC chemokine ligand 5 (CXCL5) disrupted the permeability of human brain microvascular endothelial cells via regulating p38 signal

The ischemia-reperfusion-induced damage in human brain microvascular endothelial cells (BMECs) is associated with disruption of the blood–brain barrier. CXC chemokine ligand 5 (CXCL5) reported to be up-regulated ischemic stroke. However, detailed function CXCL5 this pathological process remains largely unclear. To further analyze stroke, an oxygen–glucose deprivation model on BMECs was constructed mimic stroke condition vitro. Cell proliferation analyzed using a cell counting kit-8 (CCK-8) assay. Quantitative real-time polymerase chain reaction and western blot were utilized determine gene expression. barrier assessed fluorescently labeled dextran assay trans-epithelial/endothelial electrical resistance (TEER) technique. results indicated that antibody (anti-CXCL5) promoted cells, whereas it reduced permeability. Moreover, TEER value enhanced presence anti-CXCL5. Therefore, these findings demonstrated silencing attenuated ischemic/hypoxic-induced injury BMECs. Importantly, recombinant protein (Re-CXCL5) deeply disrupted normoxic condition. Furthermore, p38 inhibitor SB203580 significantly abolished cells. More importantly, similar also obtained under conditions Re-CXCL5. These might regulate by mediating pathway. This investigation not only understanding biological effect ischemic/hypoxic but its potential as therapeutic target for ischemic-induced disease.