摘要：

The endothelium is immunoregulatory inhat inhibitingheunctionf vasculardhesionoleculeslocks leukocyteecruitmentndhusissue inflammation.heunctionf endothelialells during leukocyteecruitment isegulatedyeactivexygenpecies (ROS)ndntioxidants. In inflammatoryitesnd lymph nodes,he endothelium istimulatedo expressdhesionoleculeshatediate leukocyteinding.pon leukocyteinding,hesedhesionoleculesctivate endothelialellignalransductionhathenlters endothelialellhapeorhepeningf passagewayshrough which leukocytesanigrate. Ifhetimulationfhispening islocked, inflammation islocked. Inhiseview, weocusnhe endothelialelldhesionolecule, vascularelldhesionolecule-1 (VCAM-1). Expressionf VCAM-1 is inducedn endothelialells during inflammatory diseasesyeveralediators, includingOS.hen, VCAM-1nhe endotheliumunctionssothcaffoldor leukocyteigrationndriggerf endothelialignalinghrough NADPHxidase-generatedOS.heseOS induceignalsorhepeningf intercellular passagewayshrough which leukocytesigrate. Ineveral inflammatory diseases, inflammation islockedy inhibitionf leukocyteindingo VCAM-1ry inhibitionf VCAM-1ignalransduction. VCAM-1ignalransductionnd VCAM-1-dependent inflammationrelockedyntioxidants.hus, VCAM-1ignaling isargetor interventiony pharmacologicalgentsndyntioxidants during inflammatory diseases.hiseview discussesOSndntioxidantunctions duringctivationf VCAM-1 expressionnd VCAM-1ignaling in inflammatory diseases.

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