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

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 Protective Effects of Bupivacaine against Kainic Acid-Induced Seizure and Neuronal Cell Death in the Rat Hippocampus

2015 ◽  
Vol 38 (4) ◽  
pp. 522-530 ◽  
Author(s):  
Kuan Ming Chiu ◽  
Chia Chan Wu ◽  
Ming Jiuh Wang ◽  
Ming Yi Lee ◽  
Su Jane Wang
Keyword(s):  
Cell Death ◽  
Kainic Acid ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Rat Hippocampus ◽  
Protective Effects

scholarly journals Protective Effects of Chunghyuldan against ROS-mediated Neuronal Cell Death in Models of Parkinson’s Disease

2010 ◽  
Vol 107 (6) ◽  
pp. 958-964 ◽  
Author(s):  
Hyo Geun Kim ◽  
Mi Sun Ju ◽  
Dong-Hyun Kim ◽  
Jongki Hong ◽  
Seung-Hun Cho ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Protective Effects

scholarly journals Protective Effects of 4-Phenylbutyrate Derivatives on the Neuronal Cell Death and Endoplasmic Reticulum Stress

2012 ◽  
Vol 35 (1) ◽  
pp. 84-90 ◽  
Author(s):  
Seisuke Mimori ◽  
Yasunobu Okuma ◽  
Masayuki Kaneko ◽  
Koichi Kawada ◽  
Toru Hosoi ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Endoplasmic Reticulum Stress ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Protective Effects
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