Neuroprotective effect of suppression of astrocytic activation by arundic acid on brain injuries in rats with acute subdural hematomas

Wajima, Daisuke; Nakagawa, Ichiro; Nakase, Hiroyuki; Yonezawa, Taiji

doi:10.1016/j.brainres.2013.05.002

Cited by 22 publications

(17 citation statements)

References 25 publications

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“…Nevertheless, it is important to point out that despite the significant increase of S100B in the tissue, it does not mean that its release was also increased, since its levels in CSF were reduced. Previous studies have shown that AA administration was able to reduce the number of cells expressing S100B protein in models of brain ischemic (Ohtani et al, 2007) and hemorrhagic stroke (Wajima et al, 2013) in adult rats. Although the present results show an increase of S100B levels in hippocampus tissue, that seems to be in disagreement with previous studies, the assessed parameters are different, while here the overall levels in the tissue is evaluated, in the cited studies only the number of cells expressing S100B is assessed, without an investigation of total tissue levels.…”

Section: Discussionmentioning

confidence: 95%

Arundic acid administration protects astrocytes, recovers histological damage and memory deficits induced by neonatal hypoxia ischemia in rats

Mari

Odorcyk

Sanches³

et al. 2019

Intl J of Devlp Neuroscience

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Introduction Perinatal hypoxia‐ischemia (HI) is one of the main causes of mortality and chronic neurological morbidity in infants and children. Astrocytes play a key role in HI progression, becoming reactive in response to the injury, releasing S100 calcium binding protein B (S100B). Since S100B inhibition seems to have neuroprotective effects on central nervous system injury models, here we evaluated the neuroprotective effects of an S100B inhibitor, arundic acid (AA) in a HI model. Methods On the 7th postnatal day, animals were submitted to the combination of common carotid artery occlusion and hypoxic atmosphere (8% O2) for 60 min. Three experiments were performed in order to: (1) define AA dose (0.1, 1 or 10 mg/kg, pre‐hypoxia i.p. injection), (2) test if repeated AA administrations (10 mg/kg at 3 time points: Pre‐hypoxia, 24 h and 48 h after HI) would improve the response and (3) investigate biochemical mechanisms involved in AA protection two days after HI. Results AA at a dose of 10 mg/kg applied before and after hypoxia, was the only treatment protocol that was able to improve HI‐induced memory deficits, to reduce tissue damage, to promote astrocytic survival in the hippocampus and to reduced extracellular release of S100B in the cerebrospinal fluid. Conclusion Overall, AA treatment showed beneficial effects on memory deficits, tissue damage, promoting astrocyte survival likely by reducing S100B release. Protection aided to astrocytes by AA treatment against HI lesion may lead to development of new therapeutic strategies that target these particular cells.

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Section: Discussionmentioning

confidence: 95%

Arundic acid administration protects astrocytes, recovers histological damage and memory deficits induced by neonatal hypoxia ischemia in rats

Mari

Odorcyk

Sanches³

et al. 2019

Intl J of Devlp Neuroscience

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“…We suggested the mechanism as follows: AQP4 in brain is the structural basis of water transportation between cerebrospinal fluid and cells, and AQP4 level can affect the activity of K ? channels on cell membrane [28,29], which breaks the balance of K ? and water balance and change the osmotic pressure, leading to further exudation of plasma proteins and water to cause brain edema.…”

Section: Discussionmentioning

confidence: 99%

Effects of High-Pressure Oxygen Therapy on Brain Tissue Water Content and AQP4 Expression in Rabbits with Cerebral Hemorrhage

Chen

Guo

et al. 2014

Cell Biochem Biophys

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To investigate the effects of different atmosphere absolutes (ATA) of high-pressure oxygen (HPO) on brain tissue water content and Aquaporin-4 (AQP4) expression in rabbits with cerebral hemorrhage. 180 New Zealand white rabbits were selected and randomly divided into normal group (n = 30), control group (n = 30) and cerebral hemorrhage group (n = 120), and cerebral hemorrhage group was divided into group A, B, C and D with 30 rabbits in each group. The groups received 1.0, 1.8, 2.0 and 2.2 ATA of HPO treatments, respectively. Ten rabbits in each group were killed at first, third and fifth day to detect the brain tissue water content and change of AQP4 expression. In cerebral hemorrhage group, brain tissue water content and AQP4 expression after model establishment were first increased, then decreased and reached the maximum on third day (p < 0.05). Brain tissue water content and AQP4 expression in control group and cerebral hemorrhage group were significantly higher than normal group at different time points (p < 0.05). In contrast, brain tissue water content and AQP4 expression in group C were significantly lower than in group A, group B, group D and control group (p < 0.05). In control group, AQP4-positive cells significantly increased after model establishment, which reached maximum on third day, and positive cells in group C were significantly less than in group A, group B and group D. We also found that AQP4 expression were positively correlated with brain tissue water content (r = 0.719, p < 0.05) demonstrated by significantly increased AQP4 expression along with increased brain tissue water content. In conclusion, HPO can decrease AQP4 expression in brain tissue of rabbits with cerebral hemorrhage to suppress the progression of brain edema and promote repairing of injured tissue. 2.0 ATA HPO exerts best effects, which provides an experimental basis for ATA selection of HPO in treating cerebral hemorrhage.

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“…72,73 Therefore, the immunohistochemical distribution of S100 should be considered when testing the effects of treatments after TBI. Those could be heparinization, 74 the use of arundic acid to suppress S100 expression in rats, 75 or the intraperitoneal application of S100 in rats. 76 Changes in the positivity of NSE-stained neurons in dependence of survival time…”

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confidence: 99%

Immunohistochemical Investigation of S100 and NSE in Cases of Traumatic Brain Injury and Its Application for Survival Time Determination

Krohn

Dreßler

Bauer

et al. 2015

Journal of Neurotrauma

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The availability of markers able to provide insight into protein changes in the central nervous system after fatal traumatic brain injury (TBI) is limited. The present study reports on the semi-quantitative assessments of the immunopositive neuroglial cells (both astrocytes and oligodendrocytes) and neurons for S100 protein (S100), as well as neuronal specific enolase (NSE), in the cerebral cortex, hippocampus, and cerebellum with regard to survival time and cause of death. Brain tissues of 47 autopsy cases with TBI (survival times ranged between several minutes and 34 d) and 10 age- and gender-matched controls (natural deaths) were examined. TBI cases were grouped according to their survival time in acute death after brain injury (ABI, n = 25), subacute death after brain injury (SBI, n = 18) and delayed death after brain injury (DBI, n = 4). There were no significant changes in the percentages of S100-stained astrocytes between TBI and control cases. The percentages of S100-positive oligodendrocytes in the pericontusional zone (PCZ) in cases with SBI were significantly lower than in controls (p < 0.05) and in the ABI group (p < 0.05). In the hippocampus, S100-positive oligodendrocytes were significantly lower in cases with ABI and SBI (both, p < 0.05), compared with controls. It is of particular interest that there were also S100-positive neurons in the PCZ and hippocampus in TBI cases after more than 2 h survival but not in ABI cases or controls. The percentages of NSE-positive neurons in the hippocampus were likewise significantly lower in cases with ABI, compared with controls (p < 0.05) but increased in cases with SBI in PCZ (p < 0.05). In conclusion, the present findings emphasize that S100 and NSE-immunopositivity might be useful for detecting the cause and process of death due to TBI. Further, S100-positivity in neurons may be helpful to estimate the survival time of fatal injuries in legal medicine.

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Neuroprotective effect of suppression of astrocytic activation by arundic acid on brain injuries in rats with acute subdural hematomas

Cited by 22 publications

References 25 publications

Arundic acid administration protects astrocytes, recovers histological damage and memory deficits induced by neonatal hypoxia ischemia in rats

Arundic acid administration protects astrocytes, recovers histological damage and memory deficits induced by neonatal hypoxia ischemia in rats

Effects of High-Pressure Oxygen Therapy on Brain Tissue Water Content and AQP4 Expression in Rabbits with Cerebral Hemorrhage

Immunohistochemical Investigation of S100 and NSE in Cases of Traumatic Brain Injury and Its Application for Survival Time Determination

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