Neuroprotection of GST, an extract of traditional Chinese herb, against ischemic brain injury induced by transient brain ischemia and reperfusion in rat hippocampus

2008 ◽  
Vol 30 (5) ◽  
pp. 471-475 ◽  
Author(s):  
Ya-Feng Sun ◽  
Dong-Sheng Pei ◽  
Qing-Xiu Zhang ◽  
Guang-Yi Zhang
Keyword(s):  
Brain Injury ◽  
Brain Ischemia ◽  
Chinese Herb ◽  
Rat Hippocampus ◽  
Ischemic Brain Injury ◽  
Ischemia And Reperfusion ◽  
Ischemic Brain ◽  
Traditional Chinese Herb

Traditional Chinese herb Dihuang Yinzi (DY) plays neuroprotective and anti-dementia role in rats of ischemic brain injury

2009 ◽  
Vol 121 (3) ◽  
pp. 444-450 ◽  
Author(s):  
Rong Hu ◽  
Chang-lin Yin ◽  
Nan Wu ◽  
Gao-yu Cui ◽  
Hui Meng ◽  
...  
Keyword(s):  
Brain Injury ◽  
Chinese Herb ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Traditional Chinese Herb

scholarly journals AMP-Dependent Hypothermia Affords Protection from Ischemic Brain Injury

2012 ◽  
Vol 33 (2) ◽  
pp. 171-174 ◽  
Author(s):  
Mirko Muzzi ◽  
Francesco Blasi ◽  
Alberto Chiarugi
Keyword(s):  
Brain Injury ◽  
Brain Ischemia ◽  
Adenosine Monophosphate ◽  
Artery Occlusion ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Stroke Treatment ◽  
Adenosine A1 ◽  
A1 Receptor ◽  
Cerebral Artery Occlusion

In light of the relevance of therapeutic hypothermia to stroke treatment, we investigated whether 5′-adenosine monophosphate (AMP)-dependent cooling affords protection from ischemic brain injury. We show that hypothermia by AMP is because of adenosine A1 receptor (A1R) activation and is not invariantly associated with hypotension. Inhibition of ecto-5′-nucleotidase-dependent constitutive degradation of brain extracellular AMP by methylene-ADP (AMPCP) also suffices to prompt A1R-dependent hypothermia without hypotension. Both intraischemic and postischemic hypothermia by AMP or AMPCP reduce infarct volumes and mortality of mice subjected to transient middle cerebral artery occlusion. Data disclose that AMP-dependent hypothermia is of therapeutic relevance to treatment of brain ischemia.

scholarly journals Astrocyte-derived interleukin-15 exacerbates ischemic brain injury via propagation of cellular immunity

2016 ◽  
Vol 114 (3) ◽  
pp. E396-E405 ◽  
Author(s):  
Minshu Li ◽  
Zhiguo Li ◽  
Yang Yao ◽  
Wei-Na Jin ◽  
Kristofer Wood ◽  
...  
Keyword(s):  
Brain Injury ◽  
Nk Cells ◽  
Brain Ischemia ◽  
Postmortem Brain ◽  
Cell Contact ◽  
Target Cells ◽  
Cell Mediated Immunity ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Interleukin 15

Astrocytes are believed to bridge interactions between infiltrating lymphocytes and neurons during brain ischemia, but the mechanisms for this action are poorly understood. Here we found that interleukin-15 (IL-15) is dramatically up-regulated in astrocytes of postmortem brain tissues from patients with ischemic stroke and in a mouse model of transient focal brain ischemia. We generated a glial fibrillary acidic protein (GFAP) promoter-controlled IL-15–expressing transgenic mouse (GFAP–IL-15tg) line and found enlarged brain infarcts, exacerbated neurodeficits after the induction of brain ischemia. In addition, knockdown of IL-15 in astrocytes attenuated ischemic brain injury. Interestingly, the accumulation of CD8+ T and natural killer (NK) cells was augmented in these GFAP–IL-15tg mice after brain ischemia. Of note, depletion of CD8+ T or NK cells attenuated ischemic brain injury in GFAP–IL-15tg mice. Furthermore, knockdown of the IL-15 receptor α or blockade of cell-to-cell contact diminished the activation and effector function of CD8+ T and NK cells in GFAP–IL-15tg mice, suggesting that astrocytic IL-15 is delivered in trans to target cells. Collectively, these findings indicate that astrocytic IL-15 could aggravate postischemic brain damage via propagation of CD8+ T and NK cell-mediated immunity.

scholarly journals Defective Neuropeptide Processing and Ischemic Brain Injury: A Study on Proprotein Convertase 2 and its Substrate Neuropeptide in Ischemic Brains

2009 ◽  
Vol 29 (4) ◽  
pp. 698-706 ◽  
Author(s):  
Shuqin Zhan ◽  
Hongbo Zhao ◽  
Aaron J White ◽  
Manabu Minami ◽  
Giuseppe Pignataro ◽  
...  
Keyword(s):  
Brain Injury ◽  
Brain Ischemia ◽  
Focal Cerebral Ischemia ◽  
Protein Biosynthesis ◽  
Mrna Level ◽  
Proteolytic Processing ◽  
Ischemic Brain Injury ◽  
Proprotein Convertase ◽  
Early Reperfusion ◽  
Ischemic Brain

Using a focal cerebral ischemia model in rats, brain ischemia-induced changes in expression levels of mRNA and protein, and activities of proprotein convertase 2 (PC2) in the cortex were examined. In situ hybridization analyses revealed a transient upregulation of the mRNA level for PC2 at an early reperfusion hour, at which the level of PC2 protein was also high as determined by immunocytochemistry and western blotting. When enzymatic activities of PC2 were analyzed using a synthetic substrate, a significant decrease was observed at early reperfusion hours at which levels of PC2 protein were still high. Also decreased at these reperfusion hours were tissue levels of dynorphin-A(1-8) (DYN-A(1-8)), a PC2 substrate, as determined by radioimmunoassay. Further examination of PC2 protein biosynthesis by metabolic labeling in cultured neuronal cells showed that in ischemic cells, the proteolytic processing of PC2 was greatly attenuated. Finally, in mice, an intracerebroventricular administration of synthetic DYN-A(1-8) significantly reduced the extent of ischemic brain injury. In mice those lack an active PC2, exacerbated brain injury was observed after an otherwise non-lethal focal ischemia. We conclude that brain ischemia attenuates PC2 and PC2-mediated neuropeptide processing. This attenuation may play a role in the pathology of ischemic brain injury.

scholarly journals Interruption of Endolysosomal Trafficking After Focal Brain Ischemia

2021 ◽  
Vol 14 ◽  
Author(s):  
Kurt Hu ◽  
Bhakta Prasad Gaire ◽  
Lalita Subedi ◽  
Awadhesh Arya ◽  
Hironori Teramoto ◽  
...  
Keyword(s):  
Brain Injury ◽  
Membrane Fusion ◽  
Brain Ischemia ◽  
Critical Role ◽  
Ischemic Brain Injury ◽  
Synaptic Connections ◽  
Attachment Protein ◽  
Ischemic Brain ◽  
Early Endosomes ◽  
The Brain

A typical neuron consists of a soma, a single axon with numerous nerve terminals, and multiple dendritic trunks with numerous branches. Each of the 100 billion neurons in the brain has on average 7,000 synaptic connections to other neurons. The neuronal endolysosomal compartments for the degradation of axonal and dendritic waste are located in the soma region. That means that all autophagosomal and endosomal cargos from 7,000 synaptic connections must be transported to the soma region for degradation. For that reason, neuronal endolysosomal degradation is an extraordinarily demanding and dynamic event, and thus is highly susceptible to many pathological conditions. Dysfunction in the endolysosomal trafficking pathways occurs in virtually all neurodegenerative diseases. Most lysosomal storage disorders (LSDs) with defects in the endolysosomal system preferentially affect the central nervous system (CNS). Recently, significant progress has been made in understanding the role that the endolysosomal trafficking pathways play after brain ischemia. Brain ischemia damages the membrane fusion machinery co-operated by N-ethylmaleimide sensitive factor (NSF), soluble NSF attachment protein (SNAP), and soluble NSF attachment protein receptors (SNAREs), thus interrupting the membrane-to-membrane fusion between the late endosome and terminal lysosome. This interruption obstructs all incoming traffic. Consequently, both the size and number of endolysosomal structures, autophagosomes, early endosomes, and intra-neuronal protein aggregates are increased extensively in post-ischemic neurons. This cascade of events eventually damages the endolysosomal structures to release hydrolases leading to ischemic brain injury. Gene knockout and selective inhibition of key endolysosomal cathepsins protects the brain from ischemic injury. This review aims to provide an update of the current knowledge, future research directions, and the clinical implications regarding the critical role of the neuronal endolysosomal trafficking pathways in ischemic brain injury.

scholarly journals Brain Ischemia as a Prelude to Alzheimer's Disease

2021 ◽  
Vol 13 ◽  
Author(s):  
Ryszard Pluta ◽  
Sławomir Januszewski ◽  
Stanisław J. Czuczwar
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Injury ◽  
White Matter ◽  
Brain Ischemia ◽  
Tau Protein ◽  
Ischemia Reperfusion ◽  
Acute Stage ◽  
Ischemic Brain Injury ◽  
Ischemic Brain

Transient ischemic brain injury causes massive neuronal death in the hippocampus of both humans and animals. This was accompanied by progressive atrophy of the hippocampus, brain cortex, and white matter lesions. Furthermore, it has been noted that neurodegenerative processes after an episode of ischemia-reperfusion in the brain can continue well-beyond the acute stage. Rarefaction of white matter was significantly increased in animals at 2 years following ischemia. Some rats that survived 2 years after ischemia developed severe brain atrophy with dementia. The profile of post-ischemic brain neurodegeneration shares a commonality with neurodegeneration in Alzheimer's disease. Furthermore, post-ischemic brain injury is associated with the deposition of folding proteins, such as amyloid and tau protein, in the intracellular and extracellular space. Recent studies on post-ischemic brain neurodegeneration have revealed the dysregulation of Alzheimer's disease-associated genes such as amyloid protein precursor, α-secretase, β-secretase, presenilin 1, presenilin 2, and tau protein. The latest data demonstrate that Alzheimer's disease-related proteins and their genes play a key role in the development of post-ischemic brain neurodegeneration with full-blown dementia in disease types such as Alzheimer's. Ongoing interest in the study of brain ischemia has provided evidence showing that ischemia may be involved in the development of the genotype and phenotype of Alzheimer's disease, suggesting that brain ischemia can be considered as a useful model for understanding the mechanisms responsible for the initiation of Alzheimer's disease.

Sign in / Sign up

Export Citation Format

Share Document