Temporal and spatial profile of caspase 8 expression and proteolysis after experimental traumatic brain injury.

摘要: Recent studies have demonstrated that the downstream caspases, such as caspase 3, act executors of apoptotic cascade after traumatic brain injury (TBI) in vivo. However, little is known about involvement caspases initiation phase apoptosis, and interaction between these initiator (e.g. caspase 8) executor experimental injuries vitro in vivo. This study investigated temporal expression cell subtype distribution procaspase 8 cleaved caspase 8 p20 from 1 h to 14 days cortical impact-induced TBI rats. Caspase 8 messenger RNA levels, estimated by semiquantitaive RT-PCR, were elevated 72 h traumatized cortex. Western blotting revealed increased immunoreactivity for proteolytically active subunit caspase 8, p20, ipsilateral cortex 6 injury, with a peak at 24 h TBI. Similar our previous studies, p18 fragment activated caspase 3 also current TBI, but peaked later timepoint (48 h) compared proteolyzed p20. Immunohistologic examinations neurons, astrocytes oligodendrocytes. Assessment DNA damage using TUNEL identified caspase 8- caspase 3-immunopositive cells apoptotic-like morphology site, immunohistochemical investigations both proteases layers 2–5 Quantitative analysis number positive exceeds expressing up impact injury. In contrast, no evidence activation was seen hippocampus, contralateral hippocampus impact. Our results provide first suggest this may occur findings contributory role mediated death