Neuroprotective effect of parthenocissin A, a natural antioxidant and free radical scavenger, in focal cerebral ischemia of rats

2009 ◽  
Vol 24 (S1) ◽  
pp. S63-S70 ◽  
Author(s):  
Shan He ◽  
Jiehong Yang ◽  
Bin Wu ◽  
Yuanjiang Pan ◽  
Haitong Wan ◽  
...  
Keyword(s):  
Free Radical ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Neuroprotective Effect ◽  
Free Radical Scavenger ◽  
Natural Antioxidant ◽  
Radical Scavenger

scholarly journals Edaravone, a free radical scavenger, mitigates both gray and white matter damages after global cerebral ischemia in rats

2009 ◽  
Vol 1279 ◽  
pp. 139-146 ◽  
Author(s):  
Kozue Kubo ◽  
Shinichi Nakao ◽  
Sachiko Jomura ◽  
Sachiyo Sakamoto ◽  
Etsuko Miyamoto ◽  
...  
Keyword(s):  
Free Radical ◽  
White Matter ◽  
Cerebral Ischemia ◽  
Free Radical Scavenger ◽  
Global Cerebral Ischemia ◽  
Radical Scavenger

Marchantin H as a Natural Antioxidant and Free Radical Scavenger

1996 ◽  
Vol 334 (1) ◽  
pp. 18-26 ◽  
Author(s):  
George Hsiao ◽  
Che-Ming Teng ◽  
Chia-Li Wu ◽  
Feng-Nien Ko
Keyword(s):  
Free Radical ◽  
Free Radical Scavenger ◽  
Natural Antioxidant ◽  
Radical Scavenger

scholarly journals Respiratory Chain Inhibition Induces Tolerance to Focal Cerebral Ischemia

1999 ◽  
Vol 19 (11) ◽  
pp. 1229-1237 ◽  
Author(s):  
F. Wiegand ◽  
W. Liao ◽  
C. Busch ◽  
S. Castell ◽  
F. Knapp ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Free Radicals ◽  
Cerebral Ischemia ◽  
Succinate Dehydrogenase ◽  
Oxygen Free Radicals ◽  
Focal Cerebral Ischemia ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Manganese Superoxide ◽  
The Brain

The authors show that the inhibitor of the succinate dehydrogenase, 3-nitroproprionic acid (3-NPA), which in high doses and with chronic administration is a neurotoxin, can induce profound tolerance to focal cerebral ischemia in the rat when administered in a single dose (20 mg/kg) 3 days before ischemia. Infarcts were approximately 70% and 35% smaller in the 3-NPA preconditioned groups of permanent and transient focal cerebral ischemia, respectively. This regimen of 3-NPA preconditioning neither induced necrosis, apoptosis, or any other histologically detectable damage to the brain, nor did it affect behavior of the animals. 3-NPA led to an immediate (1-hour) and long-lasting (3-day) decrease in succinate dehydrogenase activity (30% reduction) throughout the brain, whereas only a short metabolic impairment occurred (ATP decrease of 35% within 30 minutes, recovery within 2 hours). The authors found that 3-NPA induces a burst of reactive oxygen species and the free radical scavenger dimethylthiourea, when administered shortly before the 3-NPA stimulus, completely blocked preconditioning. Inhibition of protein synthesis with cycloheximide given at the time of 3-NPA administration completely inhibited preconditioning. The authors were unsuccessful in showing upregulation of mRNA for the manganese superoxide dismutase, and did not detect increased activities of the copper-zinc and manganese superoxide dismutases, prototypical oxygen free radicals scavenging enzymes, after 3-NPA preconditioning. The authors conclude that it is possible to pharmacologically precondition the brain against focal cerebral ischemia, a strategy that may in principal have clinical relevance. The data show the relevance of protein synthesis for tolerance, and suggests that oxygen free radicals may be critical signals in preconditioning.

scholarly journals Hypoxic but Not Ischemic Neurotoxicity of Free Radicals Revealed by Dynamic Changes in Glucose Metabolism of Fresh Rat Brain Slices on Positron Autoradiography

2000 ◽  
Vol 20 (2) ◽  
pp. 350-358 ◽  
Author(s):  
Naoto Omata ◽  
Tetsuhito Murata ◽  
Yasuhisa Fujibayashi ◽  
Atsuo Waki ◽  
Norihiro Sadato ◽  
...  
Keyword(s):  
Free Radicals ◽  
Free Radical ◽  
Rat Brain ◽  
Neuroprotective Effect ◽  
Brain Slices ◽  
Nmda Antagonist ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Dynamic Changes ◽  
K Value

Dynamic changes in the regional cerebral glucose metabolic rate induced by hypoxia/reoxygenation or ischemia/reperfusion were investigated with a positron autoradiography technique. Fresh rat brain slices were incubated with [18F]2-fluoro-2-deoxy-D-glucose ([18F]FDG) in oxygenated Krebs-Ringer solution at 36°C, and serial two-dimensional time-resolved images of [18F]FDG uptake in the slices were obtained. In the case of loading hypoxia (oxygen deprivation)/pseudoischemia (oxygen and glucose deprivation) for various periods of time, the net influx constant ( K) of [18F]FDG at preloading and after reoxygenation/pseudoreperfusion (post-loading) was quantitatively evaluated by applying the Patlak graphical method to the image data. Regardless of the brain region, with hypoxia lasting ≥20 minutes, the postloading K value was decreased compared with the unloaded control, whereas with pseudoischemia of ≤40 minutes, approximately the same level as the unloaded control was maintained. Next, the neuroprotective effect against hypoxia/pseudoischemia loading induced by the addition of a free radical scavenger or an N-methyl-D-aspartate (NMDA) antagonist was assessed by determining whether a decrease in the postloading K value was prevented. Whereas with 20-minute hypoxia, both agents exhibited a neuroprotective effect, in the case of 50-minute pseudoischemia, only the NMDA antagonist did so, with the free radical scavenger being ineffective. These results demonstrate that hypoxia causes irreversible neuronal damage within a shorter period than ischemia, with both free radicals and glutamate suggested to be involved in tandem in the neurotoxicity induced by hypoxia, whereas glutamate alone is involved in ischemic neurotoxicity.

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