scholarly journals PAF Antagonist Ginkgolide B Reduces Postischemic Neuronal Damage in Rat Brain Hippocampus

1990 ◽  
Vol 10 (1) ◽  
pp. 133-135 ◽  
Author(s):  
Heike Oberpichler ◽  
Dirk Sauer ◽  
Christine Roßberg ◽  
Hans-Dieter Mennel ◽  
Josef Krieglstein
Keyword(s):  
Beneficial Effect ◽  
Rat Brain ◽  
Neuronal Damage ◽  
Platelet Activating Factor ◽  
Ginkgolide B ◽  
Forebrain Ischemia

We investigated the effect of the known antagonist of platelet-activating factor (PAF), ginkgolide B, on postischemic neuronal damage in the rat. Neuronal necroses were evaluated in the hippocampus 7 days after a 10-min forebrain ischemia. Preischemic application of ginkgolide B (50 mg/kg p.o.) significantly reduced neuronal damage. It is suggested that the antagonism of PAF is responsible for this beneficial effect of ginkgolide B.

scholarly journals Regional Differences in Late-Onset Iron Deposition, Ferritin, Transferrin, Astrocyte Proliferation, and Microglial Activation after Transient Forebrain Ischemia in Rat Brain

1995 ◽  
Vol 15 (2) ◽  
pp. 216-226 ◽  
Author(s):  
Yoichi Kondo ◽  
Norio Ogawa ◽  
Masato Asanuma ◽  
Zensuke Ota ◽  
Akitane Mori
Keyword(s):  
Rat Brain ◽  
Parietal Cortex ◽  
Neuronal Death ◽  
Late Onset ◽  
Neuronal Damage ◽  
Pyramidal Cells ◽  
Iron Deposition ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia ◽  
Layer V

With use of iron histochemistry and immuno-histochemistry, regional changes in the appearance of iron, ferritin, transferrin, glial fibrillary acidic protein–positive astrocytes, and activated microglia were examined from 1 to 24 weeks after transient forebrain ischemia (four-vessel occlusion model) in rat brain. Expression of the C3bi receptor and the major histocompatibility complex class II antigen was used to identify microglia. Neuronal death was confirmed by hematoxylin–eosin staining only in pyramidal cells of the hippocampal CA, region, which is known as the area most vulnerable to ischemia. Perls' reaction with 3,3′-diaminobenzidine intensification revealed iron deposits in the CA, region after week 4, which gradually increased and formed clusters by week 24. Iron also deposited in layers III-V of the parietal cortex after week 8 and gradually built up as granular deposits in the cytoplasm of pyramidal cells in frontocortical layer V. An increasing astroglial reaction and the appearance of ferritin-immunopositive microglia paralleled the iron accumulation in the hippocampal CA, region, indicating that iron deposition was probably produced in the process of gliosis. Neither neuronal death nor atrophy was found in the cerebral cortex. Nevertheless, an astroglial and ferritin-immunopositive microglial reaction became evident at week 8 in the parietal cortex. On the other hand, the granular iron deposition in the pyramidal neurons of frontocortical layer V was not accompanied by any glial reaction in the chronic stage of ischemia. Three different types of iron deposition in the chronic phase after transient forebrain ischemia were shown in this study. In view of the neuronal damage caused by iron-catalyzed free radical formation, the late-onset iron deposition may be relevant to the pathogenesis of the chronic brain dysfunction seen at a late stage after cerebral ischemia.

Antisense knockdown of the glial glutamate transporter GLT-1 exacerbates hippocampal neuronal damage following traumatic injury to rat brain

2001 ◽  
Vol 13 (1) ◽  
pp. 119-128 ◽  
Author(s):  
Vemuganti L. Raghavendra Rao ◽  
Aclan Dogan ◽  
Kellie K. Bowen ◽  
Kathryn G. Todd ◽  
Robert J. Dempsey
Keyword(s):  
Rat Brain ◽  
Neuronal Damage ◽  
Traumatic Injury ◽  
Glutamate Transporter ◽  
Glial Glutamate Transporter ◽  
Antisense Knockdown

The beneficial effect of Cape gooseberry juice on carbon tetrachloride-induced neuronal damage

2016 ◽  
Vol 15 (3) ◽  
pp. 344-350 ◽  
Author(s):  
Ebtesam M. Al-Olayan ◽  
Manal F. El-Khadragy ◽  
Sawsan A. Omer ◽  
Mohamed T.M. Shata ◽  
Rami B. Kassab ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Beneficial Effect ◽  
Neuronal Damage ◽  
Cape Gooseberry

An in situ hybridization study on interleukin-1β mRNA induced by transient forebrain ischemia in the rat brain

1994 ◽  
Vol 26 (1-2) ◽  
pp. 135-142 ◽  
Author(s):  
Kazuki Yabuuchi ◽  
Masabumi Minami ◽  
Seishi Katsumata ◽  
Akira Yamazaki ◽  
Masamichi Satoh
Keyword(s):  
In Situ Hybridization ◽  
Rat Brain ◽  
Interleukin 1Β ◽  
Forebrain Ischemia ◽  
Hybridization Study ◽  
Transient Forebrain Ischemia

Hippocampal neuronal damage after transient forebrain ischemia in monkeys

1992 ◽  
Vol 29 (5) ◽  
pp. 685-690 ◽  
Author(s):  
Eiichi Tabuchi ◽  
Shunro Endo ◽  
Taketoshi Ono ◽  
Hisao Nishijo ◽  
Shougo Kuze ◽  
...  
Keyword(s):  
Neuronal Damage ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia

Production of platelet-activating factor by neuronal cells in the rat brain with cold injury

2001 ◽  
Vol 23 (6) ◽  
pp. 605-611 ◽  
Author(s):  
Takashi Tokutomi ◽  
Hikaru Maruiwa ◽  
Masaru Hirohata ◽  
Tomoya Miyagi ◽  
Minoru Shigemori
Keyword(s):  
Rat Brain ◽  
Neuronal Cells ◽  
Platelet Activating Factor ◽  
Cold Injury

CMP-Dependent Degradation of Platelet-Activating Factor (PAF) by Rat Brain Microsomes

1997 ◽  
pp. 1029-1034
Author(s):  
Ermelinda Francescangeli ◽  
Serena Porcellati ◽  
Gianfrancesco Goracci
Keyword(s):  
Rat Brain ◽  
Platelet Activating Factor ◽  
Brain Microsomes
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