scholarly journals Protective Effect of Nimodipine against Ischemic Neuronal Damage in Rat Hippocampus without Changing Postischemic Cerebral Blood Flow

1990 ◽  
Vol 10 (5) ◽  
pp. 654-659 ◽  
Author(s):  
Jörg Nuglisch ◽  
Chourouk Karkoutly ◽  
Hans Dieter Mennel ◽  
Christine Roßberg ◽  
Josef Krieglstein
Keyword(s):  
Saline Solution ◽  
Neuronal Damage ◽  
Direct Action ◽  
Neuroprotective Effect ◽  
Histological Evaluation ◽  
Ischemic Damage ◽  
Postischemic Recirculation ◽  
Bilateral Carotid ◽  
Cerebral Vasodilation ◽  
Neuroprotective Action

The purpose of the present study was to investigate the neuroprotective action of nimodipine. Furthermore, the influence of nimodipine on postischemic local CBF (LCBF) was examined. Forebrain ischemia of the rat was performed for 10 min by bilateral carotid clamping, administration of trimethaphan, and blood withdrawal to obtain an MABP of 40 mm Hg. LCBF was measured after 10 min of postischemic recirculation by injecting [14C]iodoantipyrine in saline solution. Nimodipine (0.1, 0.3, and 1.0 mg/kg) was suspended in miglyol oil and applied orally 60 min prior to ischemia. Histological evaluation was performed 7 days after ischemia. Hippocampal neuronal damage was determined as the percentage of necrotic neurons. After preischemic application of nimodipine, neuronal damage was significantly reduced in the hippocampal CA1 subfield. Postischemic LCBF was not affected by treatment with nimodipine. These findings show that nimodipine is able to protect neurons against ischemic damage. The neuroprotective effect of nimodipine was not mediated by a postischemic cerebral vasodilation, but by a direct action on the neurons.

scholarly journals Gynura procumbens Root Extract Ameliorates Ischemia-Induced Neuronal Damage in the Hippocampal CA1 Region by Reducing Neuroinflammation

Nutrients ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 181
Author(s):  
Woosuk Kim ◽  
Hyo Young Jung ◽  
Dae Young Yoo ◽  
Hyun Jung Kwon ◽  
Kyu Ri Hahn ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Neuronal Damage ◽  
Ischemia Reperfusion ◽  
Treated Group ◽  
Biological Properties ◽  
Root Extract ◽  
Ischemic Damage ◽  
Neuroprotective Effects ◽  
Hippocampal Ca1 ◽  
Vehicle Treated Group

Gynura procumbens has been used in Southeast Asia for the treatment of hypertension, hyperglycemia, and skin problems induced by ultraviolet irradiation. Although considerable studies have reported the biological properties of Gynura procumbens root extract (GPE-R), there are no studies on the effects of GPE-R in brain damages, for example following brain ischemia. In the present study, we screened the neuroprotective effects of GPE-R against ischemic damage and neuroinflammation in the hippocampus based on behavioral, morphological, and biological approaches. Gerbils received oral administration of GPE-R (30 and 300 mg/kg) every day for three weeks and 2 h after the last administration, ischemic surgery was done by occlusion of both common carotid arteries for 5 min. Administration of 300 mg/kg GPE-R significantly reduced ischemia-induced locomotor hyperactivity 1 day after ischemia. Significantly more NeuN-positive neurons were observed in the hippocampal CA1 regions of 300 mg/kg GPE-R-treated animals compared to those in the vehicle-treated group 4 days after ischemia. Administration of GPE-R significantly reduced levels of pro-inflammatory cytokines such as interleukin-1β, -6, and tumor necrosis factor-α 6 h after ischemia/reperfusion. In addition, activated microglia were significantly decreased in the 300 mg/kg GPE-R-treated group four days after ischemia/reperfusion compared to the vehicle-treated group. These results suggest that GPE-R may be one of the possible agents to protect neurons from ischemic damage by reducing inflammatory responses.

scholarly journals A Model of Global Cerebral Ischemia in C57 BL/6 Mice

2004 ◽  
Vol 24 (2) ◽  
pp. 151-158 ◽  
Author(s):  
Ichiro Yonekura ◽  
Nobutaka Kawahara ◽  
Hirofumi Nakatomi ◽  
Kazuhide Furuya ◽  
Takaaki Kirino
Keyword(s):  
Cerebral Ischemia ◽  
Genetic Background ◽  
Neuronal Degeneration ◽  
Neuronal Damage ◽  
Neuronal Injury ◽  
Genetically Engineered ◽  
Global Cerebral Ischemia ◽  
Vessel Occlusion ◽  
Bilateral Carotid ◽  
The Mean

A reproducible model of global cerebral ischemia in mice is essential for elucidating the molecular mechanism of ischemic neuronal injury. Such a model is particularly important in the mouse because many genetically engineered mutant animals are available. In C57BL/6 and SV129/EMS mice, we evaluated a three-vessel occlusion model. Occlusion of the basilar artery with a miniature clip was followed by bilateral carotid occlusion. The mean cortical cerebral blood flow was reduced to less than 10% of the preischemic value, and the mean anoxic depolarization was attained within 1 minute. In C57BL/6 mice, there was CA1 hippocampal neuronal degeneration 4 days after ischemia. Neuronal damage depended upon ischemic duration: the surviving neuronal count was 78.5 ± 8.5% after 8-minute ischemia and 8.4 ± 12.7% after 14-minute ischemia. In SV129/EMS mice, similar neuronal degeneration was not observed after 14-minute ischemia. The global ischemia model in C57BL/6 mice showed high reproducibility and consistent neuronal injury in the CA1 sector, indicating that comparison of ischemic outcome between wild-type and mutant mice could provide meaningful data using the C57BL/6 genetic background. Strain differences in this study highlight the need for consideration of genetic background when evaluating ischemia experiments in mice.

the Comparred Effect of Zyprasidone and Haloperidol at Hippocampal and Frontal Cortex at Rats

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
D. Marinescu ◽  
L. Mogoanta ◽  
T. Udristoiu
Keyword(s):  
Adverse Event ◽  
Frontal Cortex ◽  
Negative Symptoms ◽  
Structural Changes ◽  
Saline Solution ◽  
Neuroprotective Effect ◽  
Neuronal Loss ◽  
D2 Receptors ◽  
Cerebral Structure ◽  
The Brain

Background:The alteration of hippocampal and prefrontal structures is linked with schizophrenia cognitive impairment and negative symptoms. the antipsychotics can induced apoptotic mechanisms correlated with the psychopharmacological mechanism of excesive blocking of the D2 receptors. Distress determined increase of the glucocorticoid aggression wich drive to the decrease of neuroprotective capacity at the brain level.Methods:We formed 5 study lots (5 adults rats) and a control lot. the substancies were administrated intraperitoneal, daily, saline solution equivalent to: ziprasidone (1.25mg/kg/day) and haloperidole (0.20mg/kg/day), dexametasone (0.20mg/kg/day):N1 - Haloperidole; N2 - Dexametasone; N3 - Ziprasidone; N4 - Dexametasone and Haloperidole; N5 - Dexametasone and Ziprasidone; N6 -control lot.We monitorised the cardiovascular function, respiration and EPS, without signaling any serious deadly adverse event. the rats were sacrificed during the 10th day and 21th day.Results:Frontal cortex and hippocamp were the most intensely affected even since the 10-th day to the N4 (haloperidole and dexametasone) lot with massive neuronal loss at the VI, V, and IV frontal cerebral layers.The lots treated with ziprasidone presented significant lesser structural changes in frontal cortex and hippocamp, comparative to haloperidole. the lots treated with dexametasone and ziprasidone (N5) are lesser affected at the cerebral structure level.Conclusions:Haloperidole has a significant decrease in neuroprotection. Ziprasidone demonstrated an neuroprotective effect.

scholarly journals Neuroprotective Effect of Vanda roxburghii Extract in Endothelin-1 (et-1) Induced Hippocampal Ischemic Damage and Ameliorate Cognitive Deficit

2020 ◽  
Vol 54 (3) ◽  
pp. 740-749
Author(s):  
Ravi Mundugaru ◽  
Sukrant Sharma ◽  
Senthilkumar Sivanesan ◽  
Rajesh Thangarajan ◽  
Pundalik Rama Naik ◽  
...  
Keyword(s):  
Cognitive Deficit ◽  
Neuroprotective Effect ◽  
Ischemic Damage ◽  
Endothelin 1

scholarly journals Assessment of Postischemic Neurogenesis in Rats with Cerebral Ischemia and Propofol Anesthesia

2009 ◽  
Vol 110 (3) ◽  
pp. 529-537 ◽  
Author(s):  
Irina Lasarzik ◽  
Uta Winkelheide ◽  
Sonja Stallmann ◽  
Christian Orth ◽  
Astrid Schneider ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Spatial Learning ◽  
Neuronal Damage ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
High Dose ◽  
Sprague Dawley ◽  
Bilateral Carotid ◽  
Significant Difference ◽  
Treatment Naïve

Background Postischemic endogenous neurogenesis can be dose-dependently modulated by volatile anesthetics. The intravenous anesthetic propofol is used during operations with a risk of cerebral ischemia, such as neurosurgery, cardiac surgery, and vascular surgery. The effects of propofol on neurogenesis are unknown and, therefore, the object of this study. Methods Eighty male Sprague-Dawley rats were randomly assigned to treatment groups with propofol administration for 3 h: 36 mg x kg(-1) x h(-1) propofol with or without cerebral ischemia and 72 mg x kg(-1) x h(-1) propofol with or without cerebral ischemia. In addition, 7 rats with propofol administration for 6 h and 14 treatment-naive rats were investigated. Forebrain ischemia was induced by bilateral carotid artery occlusion and hemorrhagic hypotension. Animals received 5-bromo-2-deoxyuridine for 7 days. 5-Bromo-2-deoxyuridine-positive neurons were counted in the dentate gyrus after 9 and 28 days. Spatial learning in the Barnes maze and histopathologic damage of the hippocampus were analyzed. Results Propofol revealed no impact on basal neurogenesis. Cerebral ischemia increased the amount of new neurons. After 28 days, neurogenesis significantly increased in animals with low-dose propofol administered during cerebral ischemia compared with naive animals, whereas no significant difference was observed in animals with high-dose propofol during ischemia. Neuronal damage in the CA3 region was increased at 28 days with high-dose propofol. Postischemic deficits in spatial learning were not affected by propofol. Conclusions Independent effects of propofol are difficult to ascertain. Peri-ischemic propofol administration may exert secondary effects on neurogenesis by modulating the severity of histopathologic injury and thereby regenerative capacity of the hippocampus.

Leptin's neuroprotective action in experimental transient ischemic damage of the gerbil hippocampus is linked to altered leptin receptor immunoreactivity

2011 ◽  
Vol 303 (1-2) ◽  
pp. 100-108 ◽  
Author(s):  
Bing Chun Yan ◽  
Jung Hoon Choi ◽  
Ki-Yeon Yoo ◽  
Choong Hyun Lee ◽  
In Koo Hwang ◽  
...  
Keyword(s):  
Leptin Receptor ◽  
Ischemic Damage ◽  
Neuroprotective Action

scholarly journals Histological features of peritoneal lavage with ropivacaine in rats with fecal peritonitis

2012 ◽  
Vol 27 (2) ◽  
pp. 193-199 ◽  
Author(s):  
Marcos Célio Brocco ◽  
Renato Santiago Gomez ◽  
Danilo Nagib Salomão Paulo ◽  
Carlos Eduardo David de Almeida ◽  
João Florêncio de Abreu Baptista
Keyword(s):  
Saline Solution ◽  
Peritoneal Lavage ◽  
Abdominal Cavity ◽  
Group Iv ◽  
Histological Evaluation ◽  
Fecal Peritonitis ◽  
Control Groups ◽  
Histological Features ◽  
Post Surgery ◽  
And Control

PURPOSE: To evaluate the histological features in lungs, peritoneum and liver of rats subjected to fecal peritonitis and treated with peritoneal lavage with 0.2% ropivacaine. METHODS: Twenty Wistar rats were subjected to laparotomy 6 h after the fecal peritonitis induction with autogenous stool. Rats were randomly distributed into 4 groups: I - (n=5) Control, no treatment; II - (n=5) Drying of the abdominal cavity; III - (n=5) Abdominal cavity lavage with 3 ml 0.9% saline solution and drying; and IV - (n=5) Abdominal cavity lavage with 3 ml 0.2% ropivacaine and drying. The animals that died underwent necropsy, and the surviving ones were subjected to euthanasia on the 11th day post-surgery. Fragments of liver, lungs and peritoneum were removed for histological evaluation. RESULTS: The animals that received peritoneal lavage (groups III and IV) showed greater survival than the drying and control groups. Lavage with ropivacaine prevented death during the observed period. Peritoneal lavage with ropivacaine maintained the architecture of the lung, peritoneum and liver without any important histological alterations. The histopathological findings analyzed correlated with greater survival of group IV. CONCLUSION: Treatment of fecal peritonitis in rats with peritoneal lavage using 0.2% ropivacaine demonstrated a reduction in histopathological alterations related to inflammatory response and sepsis.

scholarly journals Tat-Cannabinoid Receptor Interacting Protein Reduces Ischemia-Induced Neuronal Damage and Its Possible Relationship with 14-3-3η

Cells ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 1827 ◽  
Author(s):  
Hyun Jung Kwon ◽  
Duk-Soo Kim ◽  
Woosuk Kim ◽  
Hyo Young Jung ◽  
Yeon Hee Yu ◽  
...  
Keyword(s):  
Cannabinoid Receptor ◽  
Neuronal Damage ◽  
Cell Damage ◽  
Ischemia Reperfusion ◽  
Ischemic Damage ◽  
Dependent Manner ◽  
Ht22 Cells ◽  
Concentration Dependent Manner ◽  
H2o2 Treatment ◽  
Interacting Protein

Cannabinoid receptor-interacting protein 1a (CRIP1a) binds to the C-terminal domain of cannabinoid 1 receptor (CB1R) and regulates CB1R activities. In this study, we made Tat-CRIP1a fusion proteins to enhance CRIP1a penetration into neurons and brain and to evaluate the function of CRIP1a in neuroprotection following oxidative stress in HT22 hippocampal cells and transient forebrain ischemia in gerbils. Purified exogenous Tat-CRIP1a was penetrated into HT22 cells in a time and concentration-dependent manner and prevented H2O2-induced reactive oxygen species formation, DNA fragmentation, and cell damage. Tat-CRIP1a fusion protein also ameliorated the reduction of 14-3-3η expression by H2O2 treatment in HT22 cells. Ischemia–reperfusion damage caused motor hyperactivity in the open field test of gerbils; however, the treatment of Tat-CRIP1a significantly reduced hyperactivity 1 day after ischemia. Four days after ischemia, the administration of Tat-CRIP1a restored the loss of pyramidal neurons and decreased reactive astrocytosis and microgliosis induced by ischemic damage in the hippocampal cornu Ammonis (CA)1 region. Ischemic damage decreased 14-3-3η expression in all hippocampal sub-regions 4 days after ischemia; however, the treatment of Tat-CRIP1 ameliorated the reduction of 14-3-3η expression. These results suggest that Tat-CRIP1a attenuates neuronal damage and hyperactivity induced by ischemic damage, and it restores normal expression levels of 14-3-3η protein in the hippocampus.

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