Dynamics of Polymorphonuclear Leukocyte Accumulation in Acute Cerebral Infarction and Their Correlation With Brain Tissue Damage

Stroke ◽  
1996 ◽  
Vol 27 (10) ◽  
pp. 1739-1743 ◽  
Author(s):  
S.E. Akopov ◽  
N.A. Simonian ◽  
G.S. Grigorian
Author(s):  
Sławomir Blamek ◽  
Dawid Larysz ◽  
Kornelia Ficek ◽  
Maria Sokół ◽  
Leszek Miszczyk ◽  
...  

Neurosurgery ◽  
2009 ◽  
Vol 64 (1) ◽  
pp. 156-163 ◽  
Author(s):  
Brigitte Piallat ◽  
Stéphan Chabardès ◽  
Annaelle Devergnas ◽  
Napoleon Torres ◽  
Marjolaine Allain ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Tingting Yan ◽  
Yan Zhao ◽  
Xia Zhang

Excessive alcohol consumption can lead to brain tissue damage and cognitive dysfunction. It has been shown that heavy drinking is associated with an earlier onset of neurodegenerative diseases such as Alzheimer’s disease. Acetaldehyde, the most toxic metabolite of ethanol, is speculated to mediate the brain tissue damage and cognitive dysfunction induced by the chronic excessive consumption of alcohol. However, the exact mechanisms by which acetaldehyde induces neurotoxicity are not totally understood. In this study, we investigated the cytotoxic effects of acetaldehyde in SH-SY5Y cells and found that acetaldehyde induced apoptosis of SH-SY5Y cells by downregulating the expression of antiapoptoticBcl-2andBcl-xLand upregulating the expression of proapoptoticBax. Acetaldehyde treatment led to a significant decrease in the levels of activated Akt and cyclic AMP-responsive element binding protein (CREB). In addition, acetaldehyde induced the activation of p38 mitogen-activated protein kinase (MAPK) while inhibiting the activation of extracellular signal-regulated kinases (ERKs, p44/p42MAPK). Meanwhile, acetaldehyde treatment caused an increase in the production of reactive oxygen species and elevated the oxidative stress in SH-SY5Y cells. Therefore, acetaldehyde induces cytotoxicity of SH-SY5Y cells via promotion of apoptotic signaling, inhibition of cell survival pathway, and induction of oxidative stress.


2011 ◽  
Vol 40 (8) ◽  
pp. 840-844 ◽  
Author(s):  
G. Pavlíková ◽  
R. Foltán ◽  
M. Burian ◽  
E. Horká ◽  
S. Adámek ◽  
...  

2020 ◽  
Vol 21 (8) ◽  
pp. 702-709
Author(s):  
Weilin Wu ◽  
Chenfeng Qiu ◽  
Xuewen Feng ◽  
Xiaoxiao Tao ◽  
Qian Zhu ◽  
...  

Objective: The purpose of this paper was to study the protective effect of paeoniflorin on acute cerebral ischemia. The animal model of cerebral infarction induced by Middle Cerebral Artery Occlusion (MCAO) was blocked by the suture method. Sixty SD rats were randomly divided into the shame group, MCAO group, paeoniflorin (60, 120, 240 mg/kg, respectively) and Nimodipine (NMDP) group (n = 10 per group). Methods: The rats were intragastrically administered immediately after the operation. After 7 days of gavage, the brains were decapitated at 24 h. Hematoxylin and Eosin (HE) staining was used to observe the degree of cell damage in the cerebral cortex of rats. Immunohistochemistry was used to detect silver plating and to observe changes in nerve cells. Rats in the model group showed obvious symptoms of neurological deficits, such as the ischemic morphological changed, the Malondialdehyde (MDA), Lactate Dehydrogenase (LD) content and lactate dehydrogenase (LDH) activity were significantly increased in the ischemic brain tissue, while the Superoxide Dismutase (SOD) activity was decreased. Results: The decrease in Na+-K+-ATPase activity was significantly lower than that in the sham group. The neurological symptoms and signs of MCAO in the different doses of paeoniflorin group were improved, and the neuronal edema in the cortical area was alleviated. The activities of SOD, LDH and Na+-K+-ATPase were significantly increased, and the contents of MDA and LD were decreased. Conclusion: Therefore, paeoniflorin could alleviate the degree of tissue damage in rats with acute cerebral infarction, inhabit the formation of free radicals in the brain tissue after ischemia, and reduce the degree of lipid peroxidation. Thus, the degree of cell damage was reduced greatly and a protective effect was showed on cerebral ischemia.


2008 ◽  
Vol 3 ◽  
pp. BMI.S359 ◽  
Author(s):  
Britt-Marie Stålnacke ◽  
Peter Sojka

Objectives The aim of the study was to analyse whether the controlled heading of soccer balls elicits increased serum concentrations of a biochemical marker of brain tissue damage S-100B. Methods Nineteen male soccer players were randomly divided into two groups, A and B. Group A headed a soccer ball falling from 18 m five times, while group B served as controls (no heading). Blood samples were taken before and 0.5 h, 2 h and 4 h after the heading for analysis of S-100B. Results No statistically significant (p > 0.05) increases in serum concentrations of S-100B were encountered in group A at 0.5 h (0.109 ± 0.024 μg/L), 2 h (0.098 ± 0.026 μg/L), and 4 h (0.113 ± 0.035 μg/L) when the blood samples obtained before and after the heading were compared (0.157 ± 0.134 μg/L). No statistically significant difference was found when the serum concentrations of S-100B were compared between groups A and B either before or after heading. Conclusions Heading a soccer ball dropped from a height of 18 m five times was not found to cause an increase in serum concentrations of S-100B, indicating that the impact was not sufficient to cause biochemically discernible damage of brain tissue.


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