scholarly journals Methyl-isobutyl amiloride reduces brain Lac/NAA, cell death and microglial activation in a perinatal asphyxia model

2012 ◽  
Vol 124 (5) ◽  
pp. 645-657 ◽  
Author(s):  
Nicola J. Robertson ◽  
Takenori Kato ◽  
Alan Bainbridge ◽  
Manigandan Chandrasekaran ◽  
Osuke Iwata ◽  
...  
Keyword(s):  
Cell Death ◽  
Microglial Activation ◽  
Perinatal Asphyxia ◽  
Methyl Isobutyl

scholarly journals Neonatal Mesenchymal Stem Cell Treatment Improves Myelination Impaired by Global Perinatal Asphyxia in Rats

2021 ◽  
Vol 22 (6) ◽  
pp. 3275
Author(s):  
Andrea Tapia-Bustos ◽  
Carolyne Lespay-Rebolledo ◽  
Valentina Vío ◽  
Ronald Pérez-Lobos ◽  
Emmanuel Casanova-Ortiz ◽  
...  
Keyword(s):  
Cell Death ◽  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Perinatal Asphyxia ◽  
Mrna Levels ◽  
Protein Levels ◽  
Delayed Cell Death ◽  
External Capsule ◽  
Stem Cell Treatment ◽  
Main Effects

The effect of perinatal asphyxia (PA) on oligodendrocyte (OL), neuroinflammation, and cell viability was evaluated in telencephalon of rats at postnatal day (P)1, 7, and 14, a period characterized by a spur of neuronal networking, evaluating the effect of mesenchymal stem cell (MSCs)-treatment. The issue was investigated with a rat model of global PA, mimicking a clinical risk occurring under labor. PA was induced by immersing fetus-containing uterine horns into a water bath for 21 min (AS), using sibling-caesarean-delivered fetuses (CS) as controls. Two hours after delivery, AS and CS neonates were injected with either 5 μL of vehicle (10% plasma) or 5 × 104 MSCs into the lateral ventricle. Samples were assayed for myelin-basic protein (MBP) levels; Olig-1/Olig-2 transcriptional factors; Gglial phenotype; neuroinflammation, and delayed cell death. The main effects were observed at P7, including: (i) A decrease of MBP-immunoreactivity in external capsule, corpus callosum, cingulum, but not in fimbriae of hippocampus; (ii) an increase of Olig-1-mRNA levels; (iii) an increase of IL-6-mRNA, but not in protein levels; (iv) an increase in cell death, including OLs; and (v) MSCs treatment prevented the effect of PA on myelination, OLs number, and cell death. The present findings show that PA induces regional- and developmental-dependent changes on myelination and OLs maturation. Neonatal MSCs treatment improves survival of mature OLs and myelination in telencephalic white matter.

scholarly journals Minocycline attenuates ethanol-induced cell death and microglial activation in the developing spinal cord

Alcohol ◽  
2019 ◽  
Vol 79 ◽  
pp. 25-35 ◽  
Author(s):  
Zhenhua Ren ◽  
Xin Wang ◽  
Mei Xu ◽  
Jacqueline A. Frank ◽  
Jia Luo
Keyword(s):  
Spinal Cord ◽  
Cell Death ◽  
Microglial Activation ◽  
Developing Spinal Cord

Xenon augmented hypothermia reduces early lactate/N-acetylaspartate and cell death in perinatal asphyxia

2011 ◽  
Vol 70 (1) ◽  
pp. 133-150 ◽  
Author(s):  
Stuart Faulkner ◽  
Alan Bainbridge ◽  
Takenori Kato ◽  
Manigandan Chandrasekaran ◽  
Andrew B. Kapetanakis ◽  
...  
Keyword(s):  
Cell Death ◽  
Perinatal Asphyxia

Cytoplasmic HIV-RNA in monocytes determines microglial activation and neuronal cell death in HIV-associated neurodegeneration

2014 ◽  
Vol 261 ◽  
pp. 685-697 ◽  
Author(s):  
Simon Faissner ◽  
Björn Ambrosius ◽  
Kirsten Schanzmann ◽  
Bastian Grewe ◽  
Anja Potthoff ◽  
...  
Keyword(s):  
Cell Death ◽  
Microglial Activation ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Hiv Rna

scholarly journals A New Neolignan Derivative, Balanophonin Isolated fromFirmiana simplexDelays the Progress of Neuronal Cell Death by Inhibiting Microglial Activation

2017 ◽  
Vol 25 (5) ◽  
pp. 519-527 ◽  
Author(s):  
Soo Young Lim ◽  
Lalita Subedi ◽  
Dongyun Shin ◽  
Chung Sub Kim ◽  
Kang Ro Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Microglial Activation ◽  
Neuronal Cell Death ◽  
Neuronal Cell

scholarly journals Dexmedetomidine Combined with Therapeutic Hypothermia Is Associated with Cardiovascular Instability and Neurotoxicity in a Piglet Model of Perinatal Asphyxia

2017 ◽  
Vol 39 (1-4) ◽  
pp. 156-170 ◽  
Author(s):  
Mojgan Ezzati ◽  
Go Kawano ◽  
Eridan Rocha-Ferreira ◽  
Daniel Alonso-Alconada ◽  
Jane K. Hassell ◽  
...  
Keyword(s):  
Cell Death ◽  
Therapeutic Hypothermia ◽  
Perinatal Asphyxia ◽  
White Male ◽  
Brain Regions ◽  
Resonance Spectroscopy ◽  
Large White ◽  
Whole Brain ◽  
Effective Adjunct ◽  
Fentanyl Group

The selective α2-adrenoreceptor agonist dexmedetomidine has shown neuroprotective, analgesic, anti-inflammatory, and sympatholytic properties that may be beneficial in neonatal encephalopathy (NE). As therapeutic hypothermia is only partially effective, adjunct therapies are needed to optimize outcomes. The aim was to assess whether hypothermia + dexmedetomidine treatment augments neuroprotection compared to routine treatment (hypothermia + fentanyl sedation) in a piglet model of NE using magnetic resonance spectroscopy (MRS) biomarkers, which predict outcomes in babies with NE, and immunohistochemistry. After hypoxia-ischaemia (HI), 20 large White male piglets were randomized to: (i) hypothermia + fentanyl with cooling to 33.5°C from 2 to 26 h, or (ii) hypothermia + dexmedetomidine (a loading dose of 2 μg/kg at 10 min followed by 0.028 μg/kg/h for 48 h). Whole-brain phosphorus-31 and regional proton MRS biomarkers were assessed at baseline, 24, and 48 h after HI. At 48 h, cell death was evaluated over 7 brain regions by means of transferase-mediated d-UTP nick end labeling (TUNEL). Dexmedetomidine plasma levels were mainly within the target sedative range of 1 μg/L. In the hypothermia + dexmedetomidine group, there were 6 cardiac arrests (3 fatal) versus 2 (non-fatal) in the hypothermia + fentanyl group. The hypothermia + dexmedetomidine group required more saline (p = 0.005) to maintain blood pressure. Thalamic and white-matter lactate/N-acetylaspartate did not differ between groups (p = 0.66 and p = 0.21, respectively); the whole-brain nucleotide triphosphate/exchangeable phosphate pool was similar (p = 0.73) over 48 h. Cell death (TUNEL-positive cells/mm2) was higher in the hypothermia + dexmedetomidine group than in the hypothermia + fentanyl group (mean 5.1 vs. 2.3, difference 2.8 [95% CI 0.6-4.9], p = 0.036). Hypothermia + dexmedetomidine treatment was associated with adverse cardiovascular events, even within the recommended clinical sedative plasma level; these may have been exacerbated by an interaction with either isoflurane or low body temperature. Hypothermia + dexmedetomidine treatment was neurotoxic following HI in our piglet NE model, suggesting that caution is vital if dexmedetomidine is combined with cooling following NE.

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