Cranial venous-outflow obstruction promotes neuroinflammation via ADAM17/solTNF- α/NF-κB pathway following experimental TBI
This study used an acute subdural hematoma (ASDH) model with cranial venous outflow obstruction (CVO) to explore how CVO aggravates the pathological process after TBI, especially for inflammation and tissue damage. The results suggest that intracranial venous return disorder exacerbates neurological deficits and brain edema in rats with ASDH by aggravating the destruction of endothelial cell tight junctions (TJs) proteins and promoting the expression of inflammatory factors, the activation of microglia and expression of recombinant A disintegrin and metalloprotease 17 (ADAM17) as well as the secretion of solTNF-α, a soluble form of tumor necrosis factor-alpha (TNFα), which in turn increase IκB-α ((inhibitor of the transcription factor nuclear factor-κB) and NF-κB p65. Our study revealed a molecular basis of how CVO aggravates inflammation and tissue damage.PMID:37918697 | DOI:10.1016/j.brainresbull.2023.110804
Source: Brain Research Bulletin - Category: Neurology Authors: Cheng Wang Liang Xian Shaorui Zheng Jun Li Xiangrong Chen Shousen Wang Source Type: research
More News: Bleeding | Brain | Brain Cancers | Cancer & Oncology | International Medicine & Public Health | Neurology | Study | Thrombosis