scholarly journals Goreisan Inhibits Upregulation of Aquaporin 4 and Formation of Cerebral Edema in the Rat Model of Juvenile Hypoxic-Ischemic Encephalopathy

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Yoshiaki Yano ◽  
Hajime Yano ◽  
Hisaaki Takahashi ◽  
Kouhei Yoshimoto ◽  
Shinji Tsuda ◽  
...  
Keyword(s):  
Brain Edema ◽  
Cerebral Edema ◽  
Rat Model ◽  
Prognostic Significance ◽  
Treated Group ◽  
Aquaporin 4 ◽  
Hypoxic Ischemic Encephalopathy ◽  
Mrna Levels ◽  
Aqp4 Expression ◽  
Ischemic Encephalopathy

Secondary cerebral edema regulation is of prognostic significance in hypoxic-ischemic encephalopathy (HIE), and aquaporin 4 (AQP4) plays an important role in the pathogenesis of cerebral edema. The traditional Japanese herbal medicine Goreisan relieves brain edema in adults; however, its effect and pharmacological mechanism in children are unknown. We investigated the effects of Goreisan on HIE-associated brain edema and AQP4 expression in a juvenile rat model, established by combined occlusion of middle cerebral and common carotid arteries. Magnetic resonance imaging showed that the lesion areas were significantly smaller in the Goreisan- (2 g/kg) treated group than in the nontreated (saline) group at 24 and 48 h postoperatively. AQP4 mRNA levels in the lesion and nonlesion sides were significantly suppressed in the Goreisan group compared with the nontreated group 36 h postoperatively. Western blotting revealed that levels of AQP4 protein were significantly decreased in the Goreisan group compared with the nontreated group in the lesion side 72 h postoperatively, but not at 12 or 36 h. After 14 days, the Goreisan group had a significantly better survival rate. These findings suggest that Goreisan suppresses brain edema in HIE and improves survival in juvenile rats, possibly via regulation of AQP4 expression and function.

scholarly journals Inhaled H2 or CO2 Do Not Augment the Neuroprotective Effect of Therapeutic Hypothermia in a Severe Neonatal Hypoxic-Ischemic Encephalopathy Piglet Model

2020 ◽  
Vol 21 (18) ◽  
pp. 6801
Author(s):  
Viktória Kovács ◽  
Gábor Remzső ◽  
Valéria Tóth-Szűki ◽  
Viktória Varga ◽  
János Németh ◽  
...  
Keyword(s):  
Caudate Nucleus ◽  
Therapeutic Hypothermia ◽  
Neuroprotective Effect ◽  
Fold Increase ◽  
Hypoxic Ischemic Encephalopathy ◽  
Mrna Levels ◽  
Treatment Groups ◽  
Apoptosis Inducing Factor ◽  
Co2 Treatment ◽  
Ischemic Encephalopathy

Hypoxic-ischemic encephalopathy (HIE) is still a major cause of neonatal death and disability as therapeutic hypothermia (TH) alone cannot afford sufficient neuroprotection. The present study investigated whether ventilation with molecular hydrogen (2.1% H2) or graded restoration of normocapnia with CO2 for 4 h after asphyxia would augment the neuroprotective effect of TH in a subacute (48 h) HIE piglet model. Piglets were randomized to untreated naïve, control-normothermia, asphyxia-normothermia (20-min 4%O2–20%CO2 ventilation; Tcore = 38.5 °C), asphyxia-hypothermia (A-HT, Tcore = 33.5 °C, 2–36 h post-asphyxia), A-HT + H2, or A-HT + CO2 treatment groups. Asphyxia elicited severe hypoxia (pO2 = 19 ± 5 mmHg) and mixed acidosis (pH = 6.79 ± 0.10). HIE development was confirmed by altered cerebral electrical activity and neuropathology. TH was significantly neuroprotective in the caudate nucleus but demonstrated virtually no such effect in the hippocampus. The mRNA levels of apoptosis-inducing factor and caspase-3 showed a ~10-fold increase in the A-HT group compared to naïve animals in the hippocampus but not in the caudate nucleus coinciding with the region-specific neuroprotective effect of TH. H2 or CO2 did not augment TH-induced neuroprotection in any brain areas; rather, CO2 even abolished the neuroprotective effect of TH in the caudate nucleus. In conclusion, the present findings do not support the use of these medical gases to supplement TH in HIE management.

scholarly journals hUC-MSCs Exert a Neuroprotective Effect via Anti-apoptotic Mechanisms in a Neonatal HIE Rat Model

2019 ◽  
Vol 28 (12) ◽  
pp. 1552-1559 ◽  
Author(s):  
Jianwei Xu ◽  
Zhanhui Feng ◽  
Xianyao Wang ◽  
Ying Xiong ◽  
Lan Wang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Umbilical Cord ◽  
Rat Model ◽  
Caspase 3 ◽  
Neuroprotective Effect ◽  
Hypoxic Ischemic Encephalopathy ◽  
Human Umbilical Cord ◽  
Motor Functions ◽  
Ischemic Encephalopathy

In this study, we investigated how human umbilical cord mesenchymal stem cells exerted a neuroprotective effect via antiapoptotic mechanisms in a neonatal hypoxic-ischemic encephalopathy rat model. A total of 78 10-day old (P10) rats were used. After human umbilical cord mesenchymal stem cells were collected from human umbilical cords and amplified in culture, they were administered to rat subjects 1 h after induced hypoxic-ischemic encephalopathy treatment. The short-term (48 h) and long-term (28 day) outcomes were evaluated after human umbilical cord mesenchymal stem cells treatment using neurobehavioral function assessment. Triphenyltetrazolium chloride monohydrate staining was performed at 48 h. Beclin-2 and caspase-3 levels were evaluated with Western blot and real time polymerase chain reaction at 48 h. Human umbilical cord mesenchymal stem cells were collected and administrated to hypoxic-ischemic encephalopathy pups by intracerebroventricular injection. Hypoxic-ischemic encephalopathy typically induced significant delay in development and caused impairment in both cognitive and motor functions in rat subjects. Human umbilical cord mesenchymal stem cells were shown to ameliorate hypoxic-ischemic encephalopathy-induced damage and improve both cognitive and motor functions. Although hypoxic-ischemic encephalopathy induced significant expression of caspase-3 and Beclin-2, human umbilical cord mesenchymal stem cells decreased the expression of both of them. Human umbilical cord mesenchymal stem cells may serve as a potential treatment to ameliorate brain injury in hypoxic-ischemic encephalopathy patients.

scholarly journals FASUDIL HYDROCHLORIDE EFFECTS ON EAAT2 AND ROCK2 PROTEIN EXPRESSIONS IN RAT MODEL OF NEONATAL HYPOXIC-ISCHEMIC ENCEPHALOPATHY.

2017 ◽  
Vol 5 (4) ◽  
pp. 1674-1679
Author(s):  
NdefiA ntimaYadiswaRobert ◽  
◽  
WangXian He ◽  
ZhangYa Li ◽  
ZhuZhang Long ◽  
...  
Keyword(s):  
Rat Model ◽  
Hypoxic Ischemic Encephalopathy ◽  
Protein Expressions ◽  
Ischemic Encephalopathy

Abstract WP308: Global Cerebral Edema Among Good Grade Patients with Intracerebral Hemorrhage. Results from the Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH) Study

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Shahram Majidi ◽  
Waqas I Gilani ◽  
Nauman Tariq ◽  
Haitham M Hussein ◽  
Yuko Y Palesch ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Ct Scan ◽  
Brain Edema ◽  
Cerebral Edema ◽  
Brain Volume ◽  
Prognostic Significance ◽  
Ct Scans ◽  
Total Brain Volume ◽  
Total Brain ◽  
Global Brain

INTRODUCTION: There is some evidence that injury and blood brain barrier disruption can be seen in regions distant from the hematoma in patients with intracerebral hemorrhage (ICH). Objective: To ascertain the occurrence of global brain edema in patients with ICH and to explore the relationship between patient characteristics and three month outcomes. Design: A post-hoc analysis of a traditional Phase I dose escalation multicenter prospective study recruited patients with ICH, elevated SBP≥170 mmHg, and Glasgow Coma Scale score ≥8, who presented within 6 hours of symptom onset. Computed tomographic (CT) scans at baseline, 24 hours, and any performed at later intervals were submitted to a core image laboratory. We were able to ascertain the presence and magnitude of global brain edema in 41 of 60 subjects with adequate CT scan resolution. Settings: Emergency departments and intensive care units. Primary Outcomes: We determined the total brain, hematoma, and perihematoma edema volumes from baseline, 24 hour, and 48 hour (if available) CT scans using image analysis software. The global brain edema volume was determined by subtracting the hematoma and perihematomal edema volumes from the total brain volume. Results: A total of 18 (44%) of 41 patients had global cerebral edema that developed between initial CT scan and 24 hour CT scan. The median increase in brain volume among the 18 subjects was 35 cc ranging from 0.12 cc to 296 cc. The baseline GCS score (median 15 versus 15) and hematoma volume (mean±SD; 11.5±10.3 versus 13.9±17) were similar between subjects who experienced global cerebral edema and those who did not. The initial serum glucose was higher among subjects with global cerebral edema (150.5±74.3 mg/dl verus 119.7±34.6 mg/dl). Of the 18 patients who underwent a CT scan at 48 hours, 5 had either new or worsening global cerebral edema. Three of the 18 patients with global cerebral edema underwent neurological deterioration and 1 patient died during hospitalization. Conclusions: Global cerebral edema can occur even in subjects with mild ICH. The pathophysiological basis and prognostic significance needs to be studied in future trials.

scholarly journals Effects of Melatonin and Pentoxyphilline Treatment on Newborn Rat Model of Hypoxic Ischemic Encephalopathy

2011 ◽  
Vol 70 ◽  
pp. 220-220
Author(s):  
O Soz ◽  
M K Turkmen ◽  
A Kumral ◽  
B Baykara ◽  
D C Yesilirmak ◽  
...  
Keyword(s):  
Rat Model ◽  
Hypoxic Ischemic Encephalopathy ◽  
Newborn Rat ◽  
Ischemic Encephalopathy

Transplantation of multipotent astrocytic stem cells into a rat model of neonatal hypoxic–ischemic encephalopathy

2006 ◽  
Vol 1112 (1) ◽  
pp. 99-105 ◽  
Author(s):  
Tong Zheng ◽  
Candace Rossignol ◽  
Avital Leibovici ◽  
Kevin J. Anderson ◽  
Dennis A. Steindler ◽  
...  
Keyword(s):  
Stem Cells ◽  
Rat Model ◽  
Hypoxic Ischemic Encephalopathy ◽  
Ischemic Encephalopathy
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