scholarly journals Neuroprotective Effect of YM-39558, Orotic Acid Ethylester, in Gerbil Forebrain Ischemia

1998 ◽  
Vol 76 (4) ◽  
pp. 441-444 ◽  
Author(s):  
Hiraku Akiho ◽  
Akihiko Iwai ◽  
Mika Katoh-Sudoh ◽  
Shin-ichi Tsukamoto ◽  
Kazuo Koshiya ◽  
...  
Keyword(s):  
Orotic Acid ◽  
Neuroprotective Effect ◽  
Forebrain Ischemia ◽  
Acid Ethylester

scholarly journals Pycnogenol® Supplementation Attenuates Memory Deficits and Protects Hippocampal CA1 Pyramidal Neurons via Antioxidative Role in a Gerbil Model of Transient Forebrain Ischemia

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2477
Author(s):  
Bora Kim ◽  
Tae-Kyeong Lee ◽  
Cheol Woo Park ◽  
Dae Won Kim ◽  
Ji Hyeon Ahn ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Neuroprotective Effect ◽  
Ischemic Injury ◽  
Pyramidal Cells ◽  
Acid Oxidation ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia ◽  
Ca1 Region ◽  
Pine Tree ◽  
Before And After

Pycnogenol® (an extract of the bark of French maritime pine tree) is used for dietary supplement and known to have excellent antioxidative efficacy. However, there are few reports on neuroprotective effect of Pycnogenol® supplementation and its mechanisms against ischemic injury following transient forebrain ischemia (TFI) in gerbils. Now, we examined neuroprotective effect and its mechanisms of Pycnogenol® in the gerbils with 5-min TFI, which evokes a significant death (loss) of pyramidal cells located in the cornu ammonis (CA1) region of gerbil hippocampus from 4–5 days post-TFI. Gerbils were pretreated with 30, 40, and 50 mg/kg of Pycnogenol® once a day for 7 days before TFI surgery. Treatment with 50 mg/kg, not 30 or 40 mg/kg, of Pycnogenol® potently protected learning and memory, as well as CA1 pyramidal cells, from ischemic injury. Treatment with 50 mg/kg Pycnogenol® significantly enhanced immunoreactivity of antioxidant enzymes (superoxide dismutases and catalase) in the pyramidal cells before and after TFI induction. Furthermore, the treatment significantly reduced the generation of superoxide anion, ribonucleic acid oxidation and lipid peroxidation in the pyramidal cells. Moreover, interestingly, its neuroprotective effect was abolished by administration of sodium azide (a potent inhibitor of SODs and catalase activities). Taken together, current results clearly indicate that Pycnogenol® supplementation can prevent neurons from ischemic stroke through its potent antioxidative role.

Influence of rewarming conditions after hypothermia in gerbils with transient forebrain ischemia

1999 ◽  
Vol 91 (1) ◽  
pp. 114-120 ◽  
Author(s):  
Takehiro Nakamura ◽  
Osamu Miyamoto ◽  
Shin-Ichi Yamagami ◽  
Yoshiaki Hayashida ◽  
Toshifumi Itano ◽  
...  
Keyword(s):  
Cell Damage ◽  
Cerebral Metabolism ◽  
Neuroprotective Effect ◽  
Deep Hypothermia ◽  
Moderate Hypothermia ◽  
Forebrain Ischemia ◽  
Extracellular Glutamate ◽  
Content Type ◽  
Transient Forebrain Ischemia ◽  
Fine Print

Object. Recently, several studies have demonstrated that hypothermia has a beneficial effect on clinical outcome; however, it is difficult to determine the appropriate rewarming conditions in clinical use. The purpose of the present study was to examine the influence of rewarming conditions in gerbils with transient forebrain ischemia.Methods. Ischemia was induced in the gerbils by a 5-minute bilateral common carotid artery occlusion, after which the animals were immediately subjected to moderate or deep hypothermia. After moderate hypothermia (30.5°C for 4 hours) the animals were rewarmed over standard, fast, or slow time periods. After deep hypothermia (24°C for 2 hours) the animals were rewarmed in a standard, fast, slow, or stepwise manner. Cerebral blood flow (CBF), extracellular glutamate, and lactate were monitored. Hippocampal CA1 cell damage was assessed 7 days after induction of ischemia.In animals treated with moderate hypothermia, the rewarming rate had no influence on the number of surviving neurons. However, fast rewarming from deep hypothermia (to 37°C for 30 minutes) failed to provide the neuroprotective effect of hypothermia. Furthermore, this group showed a poor recovery of CBF (p < 0.01) and, consequently, an increase in extracellular glutamate (p < 0.01) and lactate (p < 0.01) in the hippocampus.Conclusions. The results of this study indicate a transient uncoupling of CBF and cerebral metabolism during fast rewarming from deep hypothermia, whereas slow and stepwise rewarming periods were found to be useful for protection against uncoupling of CBF and cerebral metabolism during rewarming.

scholarly journals Neuroprotective Effect of Sodium Orthovanadate on Delayed Neuronal Death after Transient Forebrain Ischemia in Gerbil Hippocampus

2001 ◽  
Vol 21 (11) ◽  
pp. 1268-1280 ◽  
Author(s):  
Takayuki Kawano ◽  
Kohji Fukunaga ◽  
Yusuke Takeuchi ◽  
Motohiro Morioka ◽  
Shigetoshi Yano ◽  
...  
Keyword(s):  
Neuronal Death ◽  
Neuroprotective Effect ◽  
Delayed Neuronal Death ◽  
Intraventricular Injection ◽  
Mongolian Gerbils ◽  
Sodium Orthovanadate ◽  
Forebrain Ischemia ◽  
Neuroprotective Effects ◽  
Transient Forebrain Ischemia ◽  
Ca1 Region

In transient forebrain ischemia, sodium orthovanadate as well as insulinlike growth factor-1 (IGF-1) rescued cells from delayed neuronal death in the hippocampal CA1 region. Adult Mongolian gerbils were subjected to 5-minute forebrain ischemia. Immunoblotting analysis with anti–phospho-Akt/PKB (Akt) antibody showed that phosphorylation of Akt at serine-473 (Akt-Ser-473) in the CA1 region decreased immediately after reperfusion, and in turn transiently increased 6 hours after reperfusion. The decreased phosphorylation of Akt-Ser-473 was not observed in the CA3 region. The authors then tested effects of intraventricular injection of orthovanadate and IGF-1, which are known to activate Akt. Treatment with orthovanadate or IGF-1 30 minutes before ischemia blocked delayed neuronal death in the CA1 region. The neuroprotective effects of orthovanadate and IGF-1 were associated with preventing decreased Akt-Ser-473 phosphorylation in the CA1 region observed immediately after reperfusion. Immunohistochemical studies with the anti–phospho-Akt-Ser-473 antibody also demonstrated that Akt was predominantly in the nucleus and was moderately activated in the cell bodies and dendrites of pyramidal neurons after orthovanadate treatment. The orthovanadate treatment also prevented the decrease in phosphorylation of mitogen-activated protein kinase (MAPK). Pretreatment with combined blockade of phosphatidylinositol 3-kinase and MAPK pathways totally abolished the orthovanadate-induced neuroprotective effect. These results suggest that the activation of both Akt and MAPK activities underlie the neuroprotective effects of orthovanadate on the delayed neuronal death in the CA1 region after transient forebrain ischemia.

scholarly journals Hyperthermia-Induced Neuronal Protection against Ischemic Injury in Gerbils

1991 ◽  
Vol 11 (3) ◽  
pp. 449-452 ◽  
Author(s):  
Kazuo Kitagawa ◽  
Masayasu Matsumoto ◽  
Masafumi Tagaya ◽  
Keisuke Kuwabara ◽  
Ryuji Hata ◽  
...  
Keyword(s):  
Protective Effect ◽  
Neuronal Death ◽  
Neuroprotective Effect ◽  
Ischemic Injury ◽  
Protective Mechanism ◽  
Forebrain Ischemia ◽  
Stress Reactions ◽  
Neuronal Protection ◽  
Hyperthermic Treatment ◽  
Ca1 Area

We investigated the effect of hyperthermic pretreatment before induction of ischemia using a gerbil model of 5-min forebrain ischemia. A single hyperthermic treatment 18 h before ischemia exhibited a partial protective effect, and repetitive hyperthermic pretreatments at 18-h intervals before ischemia showed clear protection against neuronal death in the CA1 area of the hippocampus, whereas single hyperthermic treatment 3, 6, 24, or 50 h before ischemia exhibited little protective effect. This transient and cumulative neuroprotective effect of hyperthermic pretreatment strongly suggested the involvement of stress reactions after hyperthermia in the protective mechanism against ischemic neuronal death.

scholarly journals Stimulation of β2-Adrenoceptors Inhibits Apoptosis in Rat Brain after Transient Forebrain Ischemia

1998 ◽  
Vol 18 (9) ◽  
pp. 1032-1039 ◽  
Author(s):  
Yuan Zhu ◽  
Carsten Culmsee ◽  
Irina Semkova ◽  
Josef Krieglstein
Keyword(s):  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Global Ischemia ◽  
Neuroprotective Activity ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tunel Staining ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia ◽  
Dna Laddering

We have previously demonstrated that the neuroprotective effect of the β2-adrenoceptor agonist clenbuterol in vitro and in vivo was most likely mediated by an increased nerve growth factor (NGF) expression. In the present study, we examined whether clenbuterol was capable of inhibiting apoptosis caused by ischemia. Transient forebrain ischemia was performed in male Wistar rats (300 to 350 g) by clamping both common carotid arteries and reducing the blood pressure to 40 mm Hg for 10 minutes. Clenbuterol(0.1, 0.5, and 1.0 mg/kg intraperitoneally) was administered 3 hours before ischemia or immediately after ischemia. The brains were removed for histologic evaluation 7 days after ischemia. The time course of DNA fragmentation was determined 1, 2, 3 and 4 days after ischemia. Staining with terminal deoxynucleotidyl transferase(TdT)-mediated dUTP nick end-labeling (TUNEL) was used for further analysis of DNA fragments in situ 3 days after ischemia. The NGF protein was assayed by enzyme-linked immunosorbent assay. Ten-minute forebrain ischemia damaged 80% to 90% of the neurons in the hippocampal CA1 region evaluated 7 days after ischemia. Pretreatment with clenbuterol (0.5 and 1.0 mg/kg) reduced the neuronal damage by 18.1% ( P< 0.01) and 13.1% ( P < 0.05), respectively. The neuroprotective effect also was found when clenbuterol (0.5 mg/kg) was administered immediately after ischemia ( P < 0.05). The DNA laddering appeared in striatum 1 day and in hippocampus 2 days after ischemia and peaked on the third day in both regions. The DNA laddering was nearly abolished in the hippocampus and partially blocked in striatum and cortex by 0.5 mg/kg clenbuterol. These results were confirmed by TUNEL staining. Clenbuterol (0.5 mg/kg intraperitoneally) elevated the NGF protein level by 33% ( P < 0.05) in the hippocampus and 41% ( P < 0.05) in the cortex 6 hours after ischemia. Three days after ischemia, the NGF levels in these regions were no longer different between the clenbuterol-treated and control groups. This study clearly demonstrates that clenbuterol possesses a neuroprotective activity and a marked capacity to inhibit DNA degradation after global ischemia. The results suggest that clenbuterol increases NGF expression during the first hours after global ischemia and thereby protects neurons against apoptotic damage.

scholarly journals Platelet-Derived Growth Factor-BB, but Not -AA, Prevents Delayed Neuronal Death after Forebrain Ischemia in Rats

1997 ◽  
Vol 17 (10) ◽  
pp. 1097-1106 ◽  
Author(s):  
Koji Iihara ◽  
Nobuo Hashimoto ◽  
Tetsuya Tsukahara ◽  
Masahiro Sakata ◽  
Hiroji Yanamoto ◽  
...  
Keyword(s):  
Growth Factor ◽  
Neuronal Death ◽  
Pyramidal Neurons ◽  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Platelet Derived Growth Factor ◽  
Delayed Neuronal Death ◽  
Forebrain Ischemia ◽  
Ca1 Pyramidal Neurons ◽  
Neuroprotective Actions

Our previous studies demonstrated coordinate expression of platelet-derived growth factor (PDGF) -B chain and β-receptor in neurons at risk in the rat brain with focal ischemia. To clarify a role of the -B chain in the brain further, we examined whether PDGF-A or -B chain protects CA1 pyramidal neurons from delayed neuronal death after forebrain ischemia in rats. Pretreatment with PDGF-BB, but not -AA, at 120 ng/d for 2 days until forebrain ischemia was performed markedly ameliorated delayed neuronal death in CA1 pyramidal neurons on day 7 after ischemia. This neuroprotective effect of PDGF-BB was dose-dependent, and pretreatment with PDGF-BB at 240 ng/d showed almost complete inhibition of delayed neuronal death. In contrast, posttreatment with PDGF-BB at 120 ng/d starting 20 minutes after ischemia demonstrated no significant neuroprotective effect. The current study established marked neuroprotective actions of PDGF-BB in ischemic neuronal damage.

Neuroprotective effect of mivazerol, an alpha2-agonist, after transient forebrain ischemia in rats*

2005 ◽  
Vol 49 (8) ◽  
pp. 1117-1123 ◽  
Author(s):  
T. Kimura ◽  
M. Sato ◽  
T. Nishikawa ◽  
M. Tanaka ◽  
Y. Tobe ◽  
...  
Keyword(s):  
Neuroprotective Effect ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia

scholarly journals Laminarin Pretreatment Provides Neuroprotection against Forebrain Ischemia/Reperfusion Injury by Reducing Oxidative Stress and Neuroinflammation in Aged Gerbils

Marine Drugs ◽  
2020 ◽  
Vol 18 (4) ◽  
pp. 213 ◽  
Author(s):  
Joon Ha Park ◽  
Ji Hyeon Ahn ◽  
Tae-Kyeong Lee ◽  
Cheol Woo Park ◽  
Bora Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Cytokines ◽  
Pyramidal Neurons ◽  
Ischemia Reperfusion Injury ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Forebrain Ischemia ◽  
Ca1 Pyramidal Neurons ◽  
Before And After ◽  
Anti Inflammatory

Laminarin is a polysaccharide isolated from brown algae that has various biological and pharmacological activities, such as antioxidant and anti-inflammatory properties. We recently reported that pretreated laminarin exerted neuroprotection against transient forebrain ischemia/reperfusion (IR) injury when we pretreated with 50 mg/kg of laminarin once a day for seven days in adult gerbils. However, there have been no studies regarding a neuroprotective effect of pretreated laminarin against IR injury in aged animals and its related mechanisms. Therefore, in this study, we intraperitoneally inject laminarin (50 mg/kg) once a day to aged gerbils for seven days before IR (5-min transient ischemia) surgery and examine the neuroprotective effect of laminarin treatment and the mechanisms in the gerbil hippocampus. IR injury in vehicle-treated gerbils causes loss (death) of pyramidal neurons in the hippocampal CA1 field at five days post-IR. Pretreatment with laminarin effectively protects the CA1 pyramidal neurons from IR injury. Regarding the laminarin-treated gerbils, production of superoxide anions, 4-hydroxy-2-nonenal expression and pro-inflammatory cytokines [interleukin(IL)-1β and tumor necrosis factor-α] expressions are significantly decreased in the CA1 pyramidal neurons after IR. Additionally, laminarin treatment significantly increases expressions of superoxide dismutase and anti-inflammatory cytokines (IL-4 and IL-13) in the CA1 pyramidal neurons before and after IR. Taken together, these findings indicate that laminarin can protect neurons from ischemic brain injury in an aged population by attenuating IR-induced oxidative stress and neuroinflammation.

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