Long-term treadmill exercise overcomes ischemia-induced apoptotic neuronal cell death in gerbils

2005 ◽  
Vol 84 (5) ◽  
pp. 733-738 ◽  
Author(s):  
Young-Je Sim ◽  
Hong Kim ◽  
Jee-Youn Kim ◽  
Sung-Jin Yoon ◽  
Sung-Soo Kim ◽  
...  
Keyword(s):  
Cell Death ◽  
Treadmill Exercise ◽  
Neuronal Cell Death ◽  
Neuronal Cell

scholarly journals Aurintricarboxylic acid rescues PC12 cells and sympathetic neurons from cell death caused by nerve growth factor deprivation: correlation with suppression of endonuclease activity.

1991 ◽  
Vol 115 (2) ◽  
pp. 461-471 ◽  
Author(s):  
A Batistatou ◽  
L A Greene
Keyword(s):  
Cell Death ◽  
Nerve Growth Factor ◽  
Pc12 Cells ◽  
Sympathetic Neurons ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Endonuclease Activity ◽  
Term Survival ◽  
Serum Free

Past studies have shown that serum-free cultures of PC12 cells are a useful model system for studying the neuronal cell death which occurs after neurotrophic factor deprivation. In this experimental paradigm, nerve growth factor (NGF) rescues the cells from death. It is reported here that serum-deprived PC12 cells manifest an endonuclease activity that leads to internucleosomal cleavage of their cellular DNA. This activity is detected within 3 h of serum withdrawal and several hours before any morphological sign of cell degeneration or death. NGF and serum, which promote survival of the cells, inhibit the DNA fragmentation. Aurintricarboxylic acid (ATA), a general inhibitor of nucleases in vitro, suppresses the endonuclease activity and promotes long-term survival of PC12 cells in serum-free cultures. This effect appears to be independent of macromolecular synthesis. In addition, ATA promotes long-term survival of cultured sympathetic neurons after NGF withdrawal. ATA neither promotes nor maintains neurite outgrowth. It is hypothesized that the activation of an endogenous endonuclease could be responsible for neuronal cell death after neurotrophic factor deprivation and that growth factors could promote survival by leading to inhibition of constitutively present endonucleases.

scholarly journals Age-dependent effect of treadmill exercise on hemorrhage-induced neuronal cell death in rats

2013 ◽  
Vol 9 (6) ◽  
pp. 506-510 ◽  
Author(s):  
Jin-Hwan Yoon ◽  
Hee-Hyuk Lee ◽  
Eun-Surk Yi ◽  
Soon Gi Baek
Keyword(s):  
Cell Death ◽  
Treadmill Exercise ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Dependent Effect ◽  
Age Dependent

Effects of postnatal treadmill exercise on apoptotic neuronal cell death and cell proliferation of maternal-separated rat pups

2012 ◽  
Vol 34 (1) ◽  
pp. 45-56 ◽  
Author(s):  
Seung-Soo Baek ◽  
Tae-Won Jun ◽  
Ki-Jeong Kim ◽  
Mal-Soon Shin ◽  
Sun-Young Kang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Treadmill Exercise ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Rat Pups

Chrysophanol Suppressed Glutamate-Induced Hippocampal Neuronal Cell Death via Regulation of Dynamin-Related Protein 1-Dependent Mitochondrial Fission

Pharmacology ◽  
2017 ◽  
Vol 100 (3-4) ◽  
pp. 153-160 ◽  
Author(s):  
Unbin Chae ◽  
Ju-Sik Min ◽  
Hyun Hee Leem ◽  
Hyun-Shik Lee ◽  
Hong Jun Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Mitochondrial Fission ◽  
Neuronal Cell Death ◽  
Reactive Oxygen Species Generation ◽  
Neuronal Cell ◽  
Long Term Memory ◽  
Related Protein ◽  
Neuronal Function ◽  
Short And Long Term

Chrysophanic acid, or chrysophanol, is an anthraquinone found in Rheum palmatum, which was used in the preparation of oriental medicine in ancient China. The hippocampus plays a major role in controlling the activities of the short- and long-term memory. It is one of the major regions affected by excessive cell death in Alzheimer's disease. Therefore, neuronal cell-death modulation in the hippocampus is important for maintaining neuronal function. We investigated chrysophanol's effects on glutamate-induced hippocampal neuronal cell death. Chrysophanol reduced glutamate-induced cell death via suppression of proapoptotic factors and reactive oxygen species generation. Furthermore, it downregulated glutamate-induced mitochondrial fission by inhibiting dynamin-related protein 1 (Drp1) dephosphorylation. Thus, chrysophanol suppressed hippocampal neuronal cell death via inhibition of Drp1-dependent mitochondrial fission, and can be used as a therapeutic agent for treating neuronal cell death-mediated neurodegenerative diseases.

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