Cerebral ischemia induces excessive activation of poly (ADP-ribose) polymerase-1 (PARP-
1), leading to neuronal cell death and the development of post-ischemic dysfunction …

Excessive activation of poly (ADP‐ribose) polymerase‐1 (PARP‐1) is known to develop
neuronal apoptosis, necrosis and inflammation after ischaemic brain injury. Therefore …

Focal cerebral ischemia activates the nuclear protein poly (ADP-ribose) polymerase (PARP)
by single DNA strand breaks which leads to energy depletion and cell necrosis. Deletion or …

Overactivation of poly (ADP-ribose) polymerase-1 (PARP-1) in response to DNA damage is
considered to play a crucial role in the development of post-ischemic neuronal injury, such …

N-[3-(4-Oxo-3, 4-dihydro-phthalazin-1-yl) phenyl]-4-(morpholin-4-yl) butanamide
methanesulfonate monohydrate (ONO-1924H) is a novel inhibitor of poly ADP-ribose …

Traumatic brain injury produces peroxynitrite, a powerful oxidant which triggers DNA strand
breaks, leading to the activation of poly (ADP-ribose) polymerase-1 (PARP-1). We …

The activation of poly (ADP-ribose) polymerase (PARP) in the reperfused brain after
ischemia has been assumed but never has been directly presented. Our studies indicate a …

It is reported that ischemic brain injury is mediated by the activation of poly (ADP-ribose)
polymerase (PARP). In this study, we examined the pharmacological profile of KCL-440, a …

Background and purpose: Activation of poly (ADP‐ribose) polymerase (PARP) is deleterious
during cerebral ischemia. We assessed the influence of PARP activation induced by …

Abstract Poly (ADP-ribose) polymerase-1 (PARP-1) activity significantly increases during
cerebral ischemia/reperfusion. PARP-1 is an NAD+-consumption enzyme. PARP-1 …