Fig. 8: Levels and activity of necroptosis kinases increase in cerebral tissue while caspase levels and PARP1 cleavage decrease during hyperglycemia and neonatal hypoxia-ischemia (HI) brain injury in vivo.
From: Hyperglycemia potentiates a shift from apoptosis to RIP1-dependent necroptosis
Western blots from ipsilateral (ips) and contralateral (con) cerebral tissue samples taken from neonatal mice with normal glucose levels (norm) or hyperglycemia (hyper) following HI-brain injury. a Total levels of RIP1 and MLKL increase in ipsilateral tissue of hyperglycemic mice that received HI-brain injury. Total levels of RIP3 remain unchanged. b Levels of caspase-3 and caspase-7 decrease in ipsilateral tissue of hyperglycemic mice that received HI-brain injury while caspase-6 remains unchanged. PARP1 cleavage is observed in ipsilateral tissue of normal mice and decreases in hyperglycemic mice. c Phosphorylation of RIP1 (p-RIP1) increases in ipsilateral tissue from hyperglycemic mice that received HI-brain injury and is prevented by the RIP1 inhibitor, nec-1s
