Protective effects of peroxisome proliferator-activated receptors γ coactivator-1α against neuronal cell death in the hippocampal CA1 subfield after transient global ischemia

2009 ◽  
pp. NA-NA ◽  
Author(s):  
Shang-Der Chen ◽  
Tsu-Kung Lin ◽  
Ding-I Yang ◽  
Su-Ying Lee ◽  
Fu-Zen Shaw ◽  
...  
Keyword(s):  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Global Ischemia ◽  
Peroxisome Proliferator ◽  
Protective Effects ◽  
Hippocampal Ca1 ◽  
Transient Global Ischemia ◽  
Peroxisome Proliferator Activated Receptors ◽  
Hippocampal Ca1 Subfield

scholarly journals Mild Hypothermia Reduces Zinc Translocation, Neuronal Cell Death, and Mortality after Transient Global Ischemia in Mice

2002 ◽  
Vol 22 (10) ◽  
pp. 1231-1238 ◽  
Author(s):  
Daisuke Tsuchiya ◽  
Shwuhuey Hong ◽  
Sang Won Suh ◽  
Takamasa Kayama ◽  
S. Scott Panter ◽  
...  
Keyword(s):  
Cell Death ◽  
Hippocampal Neurons ◽  
Mild Hypothermia ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Global Ischemia ◽  
Doppler Flowmetry ◽  
Transient Global Ischemia ◽  
Hematoxylin Eosin ◽  
Cortical Perfusion

The authors sought to determine whether Zn2+ translocation associated with neuronal cell death occurs after transient global ischemia (TGI) in mice, as has been previously shown in rats, and to determine the effect of mild hypothermia on this reaction. To validate the TGI model, carbon-black injection and laser-Doppler flowmetry were compared in three strains of mice (C57BL/6, SV129, and HSP70 transgenic mice) to assess posterior communicating artery (PcomA) development and cortical perfusion. In C57BL/6 mice, optimal results were obtained when subjected to 20-minute TGI. Brain and rectal temperature measurements were compared to monitor hypothermia. Results of TGI were compared in normothermia (NT; 37°C) and mild hypothermia groups (HT; 33°C) by staining with Zn2+-specific fluorescent dye, N-(6-methoxy-8-quinolyl)-para-toluenesulfonamide (TSQ) and hematoxylin– eosin 72 hours after reperfusion. The Zn2+ translocation observed in hippocampus CA1, CA2, and Hilus 72 hours after 20 minutes of TGI was significantly reduced by mild hypothermia. The number of degenerating neurons in the HT group was significantly less than in the NT group. Mild hypothermia reduced mortality significantly (7.1% in HT, 42.9% in NT). Results suggest that mild hypothermia may reduce presynaptic Zn2+ release in mice, which protects vulnerable hippocampal neurons from ischemic necrosis. Future studies may further elucidate mechanisms of Zn2+-induced ischemic injury.

scholarly journals Protective effects of cyclohexenone long chain alcohols against the neuronal cell death due to calcium overloading

2000 ◽  
Vol 82 ◽  
pp. 178
Author(s):  
Mihoko Hirata ◽  
Remi Tsuchiya ◽  
Miyuki Ogawa ◽  
Nagisa Matsumoto ◽  
Masashi Yamada ◽  
...  
Keyword(s):  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Protective Effects ◽  
Calcium Overloading ◽  
Long Chain

scholarly journals 1-O-Hexyl-2,3,5-Trimethylhydroquinone Ameliorates l-DOPA-Induced Cytotoxicity in PC12 Cells

Molecules ◽  
2019 ◽  
Vol 24 (5) ◽  
pp. 867 ◽  
Author(s):  
Hyun Park ◽  
Jong Kang ◽  
Myung Lee
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Pc12 Cells ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Mitogen Activated Protein Kinase ◽  
Protective Effects ◽  
Extracellular Signal ◽  
Dopaminergic Neuronal Cell ◽  
Mitogen Activated Protein

1-O-Hexyl-2,3,5-trimethylhydroquinone (HTHQ) has previously been found to have effective anti-oxidant and anti-lipid-peroxidative activity. We aimed to elucidate whether HTHQ can prevent dopaminergic neuronal cell death by investigating the effect on l-DOPA-induced cytotoxicity in PC12 cells. HTHQ protected from both l-DOPA-induced cell death and superoxide dismutase activity reduction. When assessing the effect of HTHQ on oxidative stress-related signaling pathways, HTHQ inhibited l-DOPA-induced phosphorylation of sustained extracellular signal-regulated kinases (ERK1/2), p38 mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK1/2). HTHQ also normalized l-DOPA-reduced Bcl-2-associated death protein (Bad) phosphorylation and Bcl-2-associated X protein (Bax) expression, promoting cell survival. Taken together, HTHQ exhibits protective effects against l-DOPA-induced cell death through modulation of the ERK1/2-p38MAPK-JNK1/2-Bad-Bax signaling pathway in PC12 cells. These results suggest that HTHQ may show ameliorative effects against oxidative stress-induced dopaminergic neuronal cell death, although further studies in animal models of Parkinson’s disease are required to confirm this.

scholarly journals Peroxisome Proliferator-Activated Receptors: “Key” Regulators of Neuroinflammation after Traumatic Brain Injury

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-7 ◽  
Author(s):  
Philip F. Stahel ◽  
Wade R. Smith ◽  
Jay Bruchis ◽  
Craig H. Rabb
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuronal Cell Death ◽  
Synthetic Cannabinoids ◽  
Experimental Studies ◽  
Neuronal Cell ◽  
Peroxisome Proliferator ◽  
Therapeutic Concept ◽  
Anti Inflammatory ◽  
Peroxisome Proliferator Activated Receptors

Traumatic brain injury is characterized by neuroinflammatory pathological sequelae which contribute to brain edema and delayed neuronal cell death. Until present, no specific pharmacological compound has been found, which attenuates these pathophysiological events and improves the outcome after head injury. Recent experimental studies suggest that targeting peroxisome proliferator-activated receptors (PPARs) may represent a new anti-inflammatory therapeutic concept for traumatic brain injury. PPARs are “key” transcription factors which inhibit NFκBactivity and downstream transcription products, such as proinflammatory and proapoptotic cytokines. The present review outlines our current understanding of PPAR-mediated neuroprotective mechanisms in the injured brain and discusses potential future anti-inflammatory strategies for head-injured patients, with an emphasis on the putative beneficial combination therapy of synthetic cannabinoids (e.g., dexanabinol) with PPARαagonists (e.g., fenofibrate).

scholarly journals Caspase-3-Like Protease Activity-Independent Apoptosis at the Onset of Neuronal Cell Death in the Gerbil Hippocampus after Global Ischemia

2007 ◽  
Vol 30 (10) ◽  
pp. 1950-1953 ◽  
Author(s):  
Hiroki Shimizu ◽  
Makoto Ohgoh ◽  
Masuhiro Ikeda ◽  
Yukio Nishizawa ◽  
Hiroo Ogura
Keyword(s):  
Cell Death ◽  
Protease Activity ◽  
Caspase 3 ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Global Ischemia

Protective effects of a selective L-type voltage-sensitive calcium channel blocker, S-312-d, on neuronal cell death

2004 ◽  
Vol 67 (6) ◽  
pp. 1153-1165 ◽  
Author(s):  
Tatsurou Yagami ◽  
Keiichi Ueda ◽  
Toshiyuki Sakaeda ◽  
Naohiro Itoh ◽  
Gaku Sakaguchi ◽  
...  
Keyword(s):  
Cell Death ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Protective Effects
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