Epigallocatechin-3-gallate attenuates cerebral cortex damage and promotes brain regeneration in acrylamide-treated rats

2017 ◽  
Vol 8 (6) ◽  
pp. 2275-2282 ◽  
Author(s):  
Yin He ◽  
Dehong Tan ◽  
Yan Mi ◽  
Qian Zhou ◽  
Shujuan Ji
Keyword(s):  
Cerebral Cortex ◽  
Cell Damage ◽  
Cell Regeneration ◽  
Brain Regeneration

ACR increased the rate of nestin-positive cells implying that ACR caused cell damage, and EGCG decreased the rates of nestin-positive cells against ACR suggesting that EGCG may promote cell regeneration.

scholarly journals Identification of proteins differentially expressed by glutamate treatment in cerebral cortex of neonatal rats

2019 ◽  
Vol 35 (1) ◽  
Author(s):  
Ju-Bin Kang ◽  
Dong-Ju Park ◽  
Phil-Ok Koh
Keyword(s):  
Cerebral Cortex ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Cell Damage ◽  
Neuronal Cell ◽  
Differentially Expressed ◽  
Heat Shock Protein 60 ◽  
Sprague Dawley ◽  
Two Dimensional Gel Electrophoresis ◽  
Specific Proteins

AbstractGlutamate leads to neuronal cell damage by generating neurotoxicity during brain development. The objective of this study is to identify proteins that differently expressed by glutamate treatment in neonatal cerebral cortex. Sprague-Dawley rat pups (post-natal day 7) were intraperitoneally injected with vehicle or glutamate (10 mg/kg). Brain tissues were isolated 4 h after drug treatment and fixed for morphological study. Moreover, cerebral cortices were collected for protein study. Two-dimensional gel electrophoresis and mass spectrometry were carried out to identify specific proteins. We observed severe histopathological changes in glutamate-exposed cerebral cortex. We identified various proteins that differentially expressed by glutamate exposure. Identified proteins were thioredoxin, peroxiredoxin 5, ubiquitin carboxy-terminal hydrolase L1, proteasome subunit alpha proteins, isocitrate dehydrogenase, and heat shock protein 60. Heat shock protein 60 was increased in glutamate exposed condition. However, other proteins were decreased in glutamate-treated animals. These proteins are related to anti-oxidant, protein degradation, metabolism, signal transduction, and anti-apoptotic function. Thus, our findings can suggest that glutamate leads to neonatal cerebral cortex damage by regulation of specific proteins that mediated with various functions.

Brain lactic acidosis and ischemic cell damage: Quantitative ultrastructural changes in capillaries of rat cerebral cortex

1983 ◽  
Vol 60 (3-4) ◽  
pp. 232-240 ◽  
Author(s):  
L. Palj�rvi ◽  
S. Rehncrona ◽  
B. S�derfeldt ◽  
Y. Olsson ◽  
H. Kalimo
Keyword(s):  
Cerebral Cortex ◽  
Lactic Acidosis ◽  
Cell Damage ◽  
Rat Cerebral Cortex ◽  
Ultrastructural Changes

No changes in behaviour, nigro-striatal system neurochemistry or neuronal cell death following toxic multiple oral paraquat administration to rats

1996 ◽  
Vol 15 (7) ◽  
pp. 583-591 ◽  
Author(s):  
PS Widdowson ◽  
MJ Farnworth ◽  
R. Upton ◽  
MG Simpson
Keyword(s):  
Cerebral Cortex ◽  
Locomotor Activity ◽  
Rat Brain ◽  
Grip Strength ◽  
Cell Damage ◽  
Benzodiazepine Receptors ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Brain Regions ◽  
Nigrostriatal System

We have examined whether the widely used herbicide, paraquat (1,1'-dimethyl-4,4'dipyridylium) may accumu late in rat brain following multiple oral dosing (5 mg paraquat ion/kg/day) for 14 days and whether this dosing regime may produce signs of neurotoxicity. This dosing regime may determine whether low dose exposure to mammals may be neurotoxic. Using [14C]paraquat to measure tissue and plasma paraquat concentrations, we observed significantly higher plasma and tissue paraquat concentrations in brain, liver, lungs and kidneys of rats which received multiple doses for 14 days, as compared to paraquat concentrations in tissues of rats which received only a single paraquat dose. Brain paraquat concentrations measured 24 h after dosing were tenfold higher in rats receiving 14 daily oral doses of paraquat, as compared to concentrations follow ing a single oral dose. A neuropathological study of the rat brain yielded no evidence that multiple paraquat dosing resulted in neuronal cell damage. Particular attention was paid to the nigrostriatal system. The paraquat treated rats gained approximately 10% less body weight over the 15 day experimental period as compared with controls demon strating that the dose of paraquat was toxic to the animals. Measurements of locomotor activity using open field tests or activity monitors did not reveal any statistically significant differences between control animals and those receiving paraquat. Fore- and hind-limb grip strength were not significantly different between the paraquat treated and control rats at any time point during the dosing regime, nor was there any evidence for locomotor co ordination deficits in any of the animals receiving paraquat. Densities of dopamine D1 and D2, NMDA, muscarinic and benzodiazepine receptors in the cerebral cortex and striatum were not significantly different between controls and rats which had received multiple paraquat doses. Concentrations of catecholamine neurotransmitters in the striatum, hypothalamus and frontal cerebral cortex were also measured to examine whether there was evidence for catecholamine depletion in these brain regions. We did not observe any significant reductions in dopamine, noradrenaline or DOPAC concentrations in any brain region of paraquat treated rats as compared with controls. On the contrary, dopamine concentrations in the striatim were significantly elevated in paraquat treated animals following a 15 day paraquat dosing regime. We attribute these changes in catecholamine concentrations to the general toxicity of paraquat which produces a stress response. In conclusion, we could not find any evidence that multiple paraquat dosing can lead to changes in locomotor activity or grip strength. In addition, the absence of neuropathology or changes in neurochemistry in the nigrostriatal tract demonstrates that paraquat does not behave like MPP+(N-methyl-4-phenylpyridinium), the neurotoxic metabolite of MPTP

scholarly journals Combined Oral Administration of GABA and DPP-4 Inhibitor Prevents Beta Cell Damage and Promotes Beta Cell Regeneration in Mice

2017 ◽  
Vol 8 ◽  
Author(s):  
Wenjuan Liu ◽  
Dong Ok Son ◽  
Harry K. Lau ◽  
Yinghui Zhou ◽  
Gerald J. Prud’homme ◽  
...  
Keyword(s):  
Oral Administration ◽  
Beta Cell ◽  
Cell Damage ◽  
Cell Regeneration ◽  
Beta Cell Regeneration ◽  
Beta Cell Damage

scholarly journals Characterization of the Transcriptome of Hair Cell Regeneration in the Neonatal Mouse Utricle

2018 ◽  
Vol 51 (3) ◽  
pp. 1437-1447
Author(s):  
Jinghong Han ◽  
Hanwei Wu ◽  
Hongyi Hu ◽  
Weiqiang Yang ◽  
Hongsong Dong ◽  
...  
Keyword(s):  
Hair Cell ◽  
Cell Damage ◽  
Cell Regeneration ◽  
Newborn Mouse ◽  
Hair Cell Regeneration ◽  
Molecular Events ◽  
Balance Deficits ◽  
Pathway Analyses ◽  
Cellular Components

Background/Aims: Hearing and balance deficits are mainly caused by loss of sensory inner ear hair cells. The key signals that control hair cell regeneration are of great interest. However, the molecular events by which the cellular signals mediate hair cell regeneration in the mouse utricle are largely unknown. Methods: In the present study, we investigated gene expression changes and related molecular pathways using RNA-seq and qRT-PCR in the newborn mouse utricle in response to neomycin-induced damage. Results: There were 302 and 624 genes that were found to be up-regulated and down-regulated in neomycin-treated samples. GO and KEGG pathway analyses of these genes revealed many deregulated cellular components, molecular functions, biological processes and signaling pathways that may be related to hair cell development. More importantly, the differentially expressed genes included 9 transcription factors from the zf-C2H2 family, and eight of them were consistently down-regulated during hair cell damage and subsequent regeneration. Conclusion: Our results provide a valuable source for future studies and highlighted some promising genes, pathways or processes that may be useful for therapeutic applications.

Hair cell regeneration and recovery of the vestibuloocular reflex in the avian vestibular system

1996 ◽  
Vol 76 (5) ◽  
pp. 3301-3312 ◽  
Author(s):  
J. P. Carey ◽  
A. F. Fuchs ◽  
E. W. Rubel
Keyword(s):  
Hair Cell ◽  
Cell Density ◽  
Hair Cells ◽  
Cell Damage ◽  
Cell Loss ◽  
Average Density ◽  
Cell Regeneration ◽  
Vestibuloocular Reflex ◽  
Scanning Electron Micrographs ◽  
Hair Cell Regeneration

1. Although auditory and vestibular hair cells are known to regenerate after aminoglycoside intoxication in birds, there is only sparse evidence that the regenerated hair cells are functional. To address this issue, we examined the relation of hair cell regeneration to recovery of the vestibuloocular reflex (VOR), whose afferent signal originates at hair cells in the vestibular epithelium. Hair cell damage was produced by treating white Leghorn chicks (Gallus domesticus, 4–8 days posthatch) with streptomycin sulfate in normal saline (1,200 mg.kg-1.day-1 im) for 5 days. 2. In the 1st wk after treatment, the VOR gain was essentially 0, and hair cell density as assessed by light microscopy was approximately 40% of normal. Between the 1st and 3rd wk after treatment, the VOR was present. Although VOR gain varied considerably from one chick to another, it increased, on average, between the 1st and 3rd wk, as did the average hair cell density. At the end of 8–9 wk, the gain and phase of the VOR had returned to normal values, as had the average density of hair cells. 3. Therefore, despite the catastrophic initial effect of hair cell loss on the VOR, recovered hair cells appeared to restore the VOR completely. Average hair cell density increased with average VOR gain. VOR gain correlated better with recovery of type 1 hair cells than with recovery of type II hair cells. 4. In contrast to hair cell density, the appearance of the vestibular epithelia as assessed by hair cell stereocilia in scanning electron micrographs was a poor indicator of VOR gain. In both treated and control birds, epithelia with the same appearance could have quite different VOR gains, suggesting a variation in the functional viability of the hair cells. 5. This observation suggests that several factors, such as the repair of stereocilia, the efficacy of hair cell synapses on afferent fibers, and the extent of compensation by central vestibular pathways, may affect the recovery of VOR gain. However, our data suggest that hair cell regeneration plays an important role in this recovery.

scholarly journals Hypoglycemic Brain Injury: Phospholipids, Free Fatty Acids, and Cyclic Nucleotides in the Cerebellum of the Rat after 30 and 60 Minutes of Severe Insulin-Induced Hypoglycemia

1981 ◽  
Vol 1 (3) ◽  
pp. 267-275 ◽  
Author(s):  
Carl-David Agardh ◽  
Bo K. Siesjö
Keyword(s):  
Fatty Acids ◽  
Cerebral Cortex ◽  
Cyclic Amp ◽  
Free Fatty Acids ◽  
Cyclic Gmp ◽  
Inverse Relationship ◽  
Cell Damage ◽  
Energy State ◽  
Cellular Energy ◽  
Energy Failure

Previous results from this laboratory have shown that although prolonged severe hypoglycemia (30 or 60 min with cessation of electroencephalographic activity) leads to relatively extensive energy failure in the cerebellum. there is surprisingly little histopathologic evidence of cell damage and virtually complete sparing of the Purkinje cells. In the present study, we induced hypoglycemia of the above-mentioned durations and compared metabolic alterations in the cerebral cortex (a structure which shows extensive cell damage) and the cerebellum. The experiments were performed on rats ventilated on 70% N2O and 30% O2, and hypoglycemia was induced by insulin administration. After 30 and 60 min of hypoglycemia the majority of animals showed changes in cerebellar energy state considerably less pronounced than in the cerebral cortex. In some animals. useful amounts of glycogen remained even after 60 min of hypoglycemic coma. It is suggested that part of the resistance of the cerebellum in hypoglycemia is due to a better preserved substrate supply, probably since the cerebellum contains a higher density of glucose transport sites. However, this alone cannot explain the higher resistance of the tissue. Thus, in all 30-min animals the cerebellum showed some deterioration of cellular energy state, and after 60 min the majority had relatively extensive energy failure. Furthermore, the results obtained after 60 min of hypoglycemia suggested that some decrease in phospholipid content occurred. During hypoglycemia. the cerebellar concentrations of cyclic AMP and cyclic GMP rose. The concentration of cyclic GMP, but not that of cyclic AMP, showed an inverse relationship to the energy charge. In cerebellum, cyclic GMP rose to higher values than in the cerebral cortex, and in contrast to that in the cerebral cortex, cyclic AMP concentration in the cerebellum showed no tendency to secondary reduction with progressive deterioration of tissue energy state. During hypoglycemia, the concentrations of free fatty acids increased in the cerebellum, the values showing an inverse relationship to cellular energy state. However, the accumulation seemed less pronounced than in the cerebral cortex, even when the two structures were compared at similar degrees of deterioration of energy state. Since accumulation of polyenoic free fatty acids has been implicated in tissue damage in several adverse situations, the results hint that part of the resistance of the cerebellum to the hypoglycemic insult may be due to a better preserved Ca2+ homeostasis and/or a less pronounced activation of phospholipase A2.

scholarly journals Ornithine Decarboxylase Activity and Putrescine Levels in Reversible Cerebral Ischemia of Mongolian Gerbils: Effect of Barbiturate

1990 ◽  
Vol 10 (2) ◽  
pp. 236-242 ◽  
Author(s):  
Wulf Paschen ◽  
Joachim Hallmayer ◽  
Günter Mies ◽  
Gabriele Röhn
Keyword(s):  
Cerebral Cortex ◽  
Cerebral Ischemia ◽  
Ornithine Decarboxylase ◽  
Cell Damage ◽  
Fold Increase ◽  
Decarboxylase Activity ◽  
Mongolian Gerbils ◽  
Tissue Samples ◽  
Neuronal Necrosis ◽  
Tissue Sections

Reversible cerebral ischemia was produced in anesthetized Mongolian gerbils by occluding both common carotid arteries. After 5 min of ischemia, brains were recirculated for 8 or 24 h. Treated animals received a single intraperitoneal injection of pentobarbitol (50 mg/kg) immediately after the anuerysm clips were removed. At the end of the experiments, animals were reanesthetized and their brains frozen in situ. Tissue samples were taken from the cerebral cortex, lateral striatum, CA1 subfield of the hippocampus, thalamus, and cerebellum for measuring ornithine decarboxylase (ODC) activity and putrescine levels. In addition, 20-μm-thick coronal tissue sections were taken from the level of the striatum and stained with hematoxylin/eosin for evaluating the extent of ischemic neuronal necrosis in the lateral striatum. In control animals ODC activity and putrescine levels amounted, respectively, to 0.32 ± 0.03 nmol/g/h and 10.2 ±0.5 nmol/g in the cerebral cortex; 0.34 ± 0.02 nmol/g/h and 12.8 ± 0.5 nmol/g in the lateral striatum; 0.58 ± 0.05 nmol/g/h and 10.5 ± 0.7 nmol/g in the hippocampal CA1 subfield; 0.35 ± 0.01 nmol/g/h and 9.8 ± 0.4 nmol/g in the thalamus; and 0.25 ± 0.01 nmol/g/h and 8.3 ± 0.6 nmol/g in the cerebellum. After 5 min cerebral ischemia and 8 h recirculation, a significant 7- to 16-fold increase in ODC activity was observed in all forebrain structures studied. Following 24 h recirculation, ODC activity normalized in the cortex, striatum, and thalamus but was still significantly above control values in the hippocampal CA1 subfield. In the cerebellum ODC activity did not change significantly. Putrescine levels were significantly increased in all forebrain structures after 8 h (two- to threefold) and even more after 24 h recirculation (up to fivefold). In barbiturate-treated animals, ODC activity was not significantly changed in relation to untreated ones. There was, however, a trend to higher activity in the cerebral cortex, lateral striatum, and hippocampal CA1 subfield. Barbiturate did not produce a significant effect on postischemic putrescine levels except in the CA1 subfield. Here the putrescine content of treated animals was significantly below that found in untreated ones. In the lateral striatum, severe cell damage (>90% of neurons were necrotic) was observed in 5 of 12 untreated animals but in none of the barbiturate-treated ones (<10% of neurons necrotic). In animals with severe cell necrosis in the lateral striatum, putrescine levels amounted to 70.9 ± 3.4 nmol/g but to only 32.0 ± 2.9 nmol/g in animals in which <10% of neurons were affected (p ⩽ 0.001).

scholarly journals Hypoglycemic Brain Injury: Metabolic and Structural Findings in Rat Cerebellar Cortex during Profound Insulin-Induced Hypoglycemia and in the Recovery Period following Glucose Administration

1981 ◽  
Vol 1 (1) ◽  
pp. 71-84 ◽  
Author(s):  
C.-D. Agardh ◽  
H. Kalimo ◽  
Y. Olsson ◽  
B. K. Siesjö
Keyword(s):  
Cerebral Cortex ◽  
Structural Changes ◽  
Granule Cells ◽  
Cell Damage ◽  
Energy State ◽  
Molecular Layer ◽  
Recovery Period ◽  
Light And Electron Microscopy ◽  
Neuronal Cell ◽  
Endogenous Substrates

Previous results have shown that severe, prolonged hypoglycemia leads to neuronal cell damage in, among other structures, the cerebral cortex and the hippocampus but not the cerebellum. In order to study whether or not this sparing of cerebellar cells is due to preservation of cerebellar energy stores, hypoglycemia of sufficient severity to abolish spontaneous EEG activity was induced for 30 and 60 min. At the end of these periods of hypoglycemia, as well as after a 30 min recovery period, cerebellar tissue was sampled for biochemical analyses or for histopathological analyses by means of light and electron microscopy. After 30 min of hypoglycemia, the cerebellar energy state, defined in terms of the phosphocreatine, ATP, ADP, and AMP concentrations, was better preserved than in the cerebral cortex. After 60 min, gross deterioration of cerebellar energy state was observed in the majority of animals, and analyses of carbohydrate metabolites and amino acids demonstrated extensive consumption of endogenous substrates. In spite of this metabolic disturbance, histopathologic alterations were surprisingly discrete. After 30 min, no clear structural changes were observed. After 60 min, only small neurons in the molecular layer (basket cells) were affected, while Purkinje cells and granule cells showed few signs of damage. The results support our previous conclusion that the pathogenesis of cell damage in hypoglycemia is different from that in hypoxia-ischemia and indicate that other mechanisms than energy failure must contribute to neuronal cell damage in the brain.

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