Ablation of caspase-1 protects against TBI-induced pyroptosis in vitro and in vivo.

ABSTRACT: BACKGROUND:Traumatic brain injury (TBI) is a critical public health and socioeconomic problem throughout the world. Inflammation-induced secondary injury is one of the vital pathogenic parameters of TBI. Molecular signaling cascades of pyroptosis, a specific type of cellular necrosis, are key drivers of TBI-induced inflammation. METHODS:In this study, mice with genetically ablated caspase-1 (caspase-1-/-) were subjected to controlled cortical impact injury in vivo, and primary neuron deficient in caspase-1 through siRNA knockdown and pharmacologic inhibition was stimulated by mechanical scratch, equiaxial stretch, and LPS/ATP in vitro. We evaluated the effects of caspase-1 deficiency on neurological deficits, inflammatory factors, histopathology, cell apoptosis, and pyroptosis. RESULTS:Dur

SUBMITTER: Liu W 

PROVIDER: S-EPMC5817788 | biostudies-literature | 2018 Feb

REPOSITORIES: biostudies-literature