Dihydroartemisinin protects blood–brain barrier permeability during sepsis by inhibiting the transcription factor SNAI1. (24th June 2022)

• Record Type: Journal Article
• Authors: Liu, Fuhong; Liu, Jing; Xiang, Hongjie; Sun, Zongguo; Li, Yan; Li, Xiao; Liu, Yanjun; Liu, Ju
• Is Part Of: Clinical and experimental pharmacology and physiology. Volume 49:Number 9(2022)
• Page Start: 979
• Page End: 987
• Publication Date: 2022-06-24
• Subjects: blood–brain barrier -- dihydroartemisinin -- occludin -- Qinghao -- sepsis -- SNAI1; Clinical pharmacology -- Periodicals; Pharmacology, Experimental -- Periodicals; Physiology, Experimental -- Periodicals; Physiology, Pathological -- Periodicals; 615.1
• DOI: 10.1111/1440-1681.13683
• Languages: English
• ISSNs: 0305-1870

Abstract

Abstract: Blood–brain barrier (BBB) injury is involved in the pathogenesis of sepsis‐associated encephalopathy. In this study, we used dihydroartemisinin (DHA), a derivative of artemisinin, to treat a cecal ligation and puncture (CLP)‐induced mouse sepsis model and a tumour necrosis factor α (TNF‐α)‐stimulated human cerebral microvessel endothelial cells (hCMEC)/D3 cell line. We found that DHA decreased BBB permeability and increased the expression of the tight junction protein occludin (OCLN) in the CLP model. In hCMEC/D3 cells, DHA decreased TNF‐α‐induced hyperpermeability and increased the expression of OCLN. DHA also repressed SNAI1 expression in the CLP mouse model and in TNF‐α‐stimulated hCMEC/D3 cells. These data suggest that DHA protects BBB permeability during sepsis by stimulating the expression of OCLN, by downregulating the expression of the SNAI1 transcription factor. Abstract :