KR-31378 protects neurons from ischemia–reperfusion brain injury by attenuating lipid peroxidation and glutathione loss

Kim, Sun-Ok; Cho, In Sun; Gu, Hee Kyoung; Lee, Dong Ha; Lim, Hong; Yoo, Sung‐Eun

doi:10.1016/j.ejphar.2003.12.037

Cited by 18 publications

(4 citation statements)

References 44 publications

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“…The increase in lipid peroxidation obtained in the present work may be referred to the overstimulation of excitatory amine receptors during ischemia, which results in activation of lipases and phospholipases with the consequent changes in membrane phospholipid composition, permeability, and fluidity, thus decreasing the integrity of the plasma membrane [45][46][47][48][49].…”

Section: Discussionmentioning

confidence: 66%

Effect of MAO-B Inhibition against Ischemia-induced Oxidative Stress in the Rat Brain

Seif-El-Nasr¹,

Atia²,

Abdelsalam³

2011

Arzneimittelforschung

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An increasing number of reports suggest the involvement of oxidative stress in neurodegenerative diseases where the increased formation of reactive oxygen species (ROS) leads to neuronal damage and cell death. Dopamine may contribute to neurodegenerative disorders such as Parkinson's disease and ischemia/reperfusion-induced damage. Monoamine oxidase (MAO) enzyme (particularly MAO-B) is responsible for metabolizing dopamine and plays an important role in oxidative stress through altering the redox state of neuronal and glial cells. MAO participates in the generation of hydroxyl radicals during ischemia/reperfusion. This suggests the possible use of MAO inhibitors as neuroprotective agents for treating ischemic injury. The protective effect of deprenyl (N-methyl-N-(1-methyl-2-phenyl-ethyl)-prop-2-yn-1-amine, CAS 14611-51-9) (2 and 10 mg/kg), a MAO-B inhibitor, and beta-carotene (10 and 20 mg/kg), a natural antioxidant, was examined in a rat model of cerebral ischemia. Ischemia was induced in rats by bilateral carotid artery occlusion for 1 h followed by declamping for another hour. The effect of the drugs on the brain activity of lactate dehydrogenase (LDH) and some of the oxidative stress biomarkers such as brain activity of superoxide dismutase (SOD) and catalase (CAT) enzymes and brain malondialdehyde (MDA) content was determined. In addition, the content of catecholamines such as noradrenaline (NA) and dopamine (DA) was determined. Deprenyl decreased the ischemia-induced elevation of LDH activity and MDA content and normalized the SOD activity. In addition, deprenyl increased the CAT activity back to normal, and increased the noradrenaline and dopamine content in the brain of rats. Beta-carotene administration ameliorated the effect of ischemia followed by reperfusion (I/R) demonstrated as decreasing the LDH activity and MDA content and by increasing the SOD activity. The drug also increased CAT activity in the brain of rats. However, beta-carotene did not alter the NA and DA content. These results indicate that deprenyl protected the rat brains against the ischemia-induced oxidative damage, an effect which might be explained through multiple mechanisms, possibly due to reduction of dopamine catabolism with a subsequent increased activity on dopaminergic D2 receptors and suppressing the action of ROS as well.

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Section: Discussionmentioning

confidence: 66%

Effect of MAO-B Inhibition against Ischemia-induced Oxidative Stress in the Rat Brain

Seif-El-Nasr¹,

Atia²,

Abdelsalam³

2011

Arzneimittelforschung

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“…Brain edema in ischemic and hemorrhagic stroke is associated with production of reactive oxygen species (ROS) and resultant oxidative stress [1,2]. Endogenous and exogenous anti-oxidants reduce edema formation and brain damage following ischemia and reperfusion [1,3-5] and intracerebral hemorrhage [2,6]. Reactive oxygen species (ROS) may directly precipitate brain swelling without inducing ischemia or blood-brain barrier injury during intracranial hemorrhage and excitotoxic injury [7,8].…”

Section: Introductionmentioning

confidence: 99%

Glutamate receptor-mediated taurine release from the hippocampus during oxidative stress

Tucker

Olson

2010

J Biomed Sci

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BackgroundHippocampal slices swell and release taurine during oxidative stress. The influence of cellular signalling pathways on this process is unclear. Glutamate signalling can facilitate volume regulation in other CNS preparations. Therefore, we hypothesize activation of taurine release by oxidative stress results from tissue swelling and is coupled to activation of glutamate receptors.MethodsRat hippocampi were incubated at room temperature for 2 hr in artificial cerebrospinal fluid (aCSF) equilibrated with 95% O2 plus 5% CO2. For some slices, 1 mM taurine was added to the aCSF to maintain normal tissue taurine content. Slices then were perfused with aCSF at 35° C and baseline data recorded before 2 mM H2O2 was added. For some studies, mannitol or inhibitors of glutamate receptors or the volume-regulated anion channel (VRAC) were added before and during H2O2 treatment. The intensity of light transmitted through the slice (the intrinsic optical signal, IOS) was determined at 1-min intervals. Samples of perfusate were collected at 2-min intervals and amino acid contents determined by HPLC. Data were analyzed by repeated measures ANOVA and post hoc Dunnett’s test with significance indicated for p<0.05.ResultsIOS of slices prepared without taurine treatment increased significantly by 3.3±1.3% (mean±SEM) during oxidative stress. Little taurine was detected in the perfusate of these slices and the rate of taurine efflux did not change during H2O2 exposure. The α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate antagonist, 25 µM CNQX, but not the N-methyl-D-aspartate (NMDA) receptor antagonist, 10 µM MK-801, inhibited the increase in IOS during H2O2 treatment. Taurine-treated slices exposed to H2O2 showed no change in IOS; however, taurine efflux increased by 335±178%. When these slices were perfused with hypertonic aCSF (350 mOsm) or exposed to the VRAC inhibitor, 20 µM DCPIB, no increase in the taurine efflux rate was observed during H2O2 exposure. Taurine-treated slices perfused with 10 µM MK-801 during H2O2 exposure showed a 4.6±1.9% increase in IOS but no increase in the taurine efflux rate.ConclusionsTaurine efflux via VRAC is critical for volume regulation of hippocampal slices exposed to oxidative stress. This increased taurine efflux does not result from direct activation of the taurine release pathway by H2O2. NMDA receptor activation plays an important role in taurine release during oxidative stress.

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“…Mushroom polysaccharides and glycoproteins have demonstrated anti-tumoral, hepatoprotective, antiviral and antibacterial effects mostly in animal systems, (Wasser and Weis, 1999;Wasser and Didukh, 2005) as well as the ability to protect animal liver from aflatoxicosis (Slamenova et al, 2003). Protein-bound polysaccharide (Polysaccharide K, PSK) and polysaccharopeptide (PSP) from T. versicolor (Maeda et al, 1974;Chihara, 1990Chihara, , 1992Kim et al, 1999;Sia and Candlish, 1999;Fisher and Yang, 2002) are among the most studied. Their action, tested mostly in animal and in vitro models, seems to lie in a stimulation of the host immune response through the activation of lymphocyte cells in addition to a direct control of the peroxidative events and the radical cascade (Yuan et al, 1996;Slamenova et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Trametes versicolor: A possible tool for aflatoxin control

Zjalić¹,

Reverberi²,

Ricelli

et al. 2006

International Journal of Food Microbiology

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KR-31378 protects neurons from ischemia–reperfusion brain injury by attenuating lipid peroxidation and glutathione loss

Cited by 18 publications

References 44 publications

Effect of MAO-B Inhibition against Ischemia-induced Oxidative Stress in the Rat Brain

Effect of MAO-B Inhibition against Ischemia-induced Oxidative Stress in the Rat Brain

Glutamate receptor-mediated taurine release from the hippocampus during oxidative stress

Trametes versicolor: A possible tool for aflatoxin control

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