diamide and Brain-Ischemia

diamide has been researched along with Brain-Ischemia* in 1 studies

Other Studies

1 other study(ies) available for diamide and Brain-Ischemia

Article	Year
Post-treatment with a novel PARG inhibitor reduces infarct in cerebral ischemia in the rat. Brain research, 2003, Jul-18, Volume: 978, Issue:1-2 Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide (NAD(+)) by poly(ADP-ribose) polymerase (PARP) and degraded by poly(ADP-ribose) glycohydrolase (PARG). Overactivation of the poly(ADP-ribose) pathway increases nicotinamide and decreases cellular NAD(+)/ATP, which leads to cell death. Blocking poly(ADP-ribose) metabolism by inactivating PARP has been shown to reduce ischemia injury. We investigated whether disrupting the poly(ADP-ribose) cycle by PARG inhibition could achieve similar protection. We demonstrate that either pre- or post-ischemia treatment with 40 mg/kg of N-bis-(3-phenyl-propyl)9-oxo-fluorene-2,7-diamide, a novel PARG inhibitor, significantly reduces brain infarct volumes by 40-53% in a rat model of focal cerebral ischemia. Our result provides the first evidence that PARG inhibitors can ameliorate ischemic brain damage in vivo, in support of PARG as a new therapeutic target for treating ischemia injury. Topics: Animals; Brain; Brain Ischemia; Cerebral Infarction; Coloring Agents; Diamide; Enzyme Inhibitors; Glycoside Hydrolases; Infarction, Middle Cerebral Artery; Male; Rats; Rats, Sprague-Dawley; Reperfusion; Tetrazolium Salts; Time Factors	2003

Article

Year

Post-treatment with a novel PARG inhibitor reduces infarct in cerebral ischemia in the rat.

Brain research, 2003, Jul-18, Volume: 978, Issue:1-2

Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide (NAD(+)) by poly(ADP-ribose) polymerase (PARP) and degraded by poly(ADP-ribose) glycohydrolase (PARG). Overactivation of the poly(ADP-ribose) pathway increases nicotinamide and decreases cellular NAD(+)/ATP, which leads to cell death. Blocking poly(ADP-ribose) metabolism by inactivating PARP has been shown to reduce ischemia injury. We investigated whether disrupting the poly(ADP-ribose) cycle by PARG inhibition could achieve similar protection. We demonstrate that either pre- or post-ischemia treatment with 40 mg/kg of N-bis-(3-phenyl-propyl)9-oxo-fluorene-2,7-diamide, a novel PARG inhibitor, significantly reduces brain infarct volumes by 40-53% in a rat model of focal cerebral ischemia. Our result provides the first evidence that PARG inhibitors can ameliorate ischemic brain damage in vivo, in support of PARG as a new therapeutic target for treating ischemia injury.

Topics: Animals; Brain; Brain Ischemia; Cerebral Infarction; Coloring Agents; Diamide; Enzyme Inhibitors; Glycoside Hydrolases; Infarction, Middle Cerebral Artery; Male; Rats; Rats, Sprague-Dawley; Reperfusion; Tetrazolium Salts; Time Factors

2003