scholarly journals Protective effects of adenosine on apoptotic neuronal cell death in cultured cortical neurons

2000 ◽  
Vol 82 ◽  
pp. 182
Author(s):  
Yutaka Tamura ◽  
Taizo Fukui ◽  
Megumi Kajikawa ◽  
Mikiko Omoto ◽  
Hirohito Shiomi
2008 ◽  
Vol 13 (3-4) ◽  
pp. 163-172 ◽  
Author(s):  
Yushan Wang ◽  
M. Tracy Weiss ◽  
Junfei Yin ◽  
Catherine C. Tenn ◽  
Peggy D. Elson ◽  
...  

2000 ◽  
Vol 82 ◽  
pp. 178
Author(s):  
Mihoko Hirata ◽  
Remi Tsuchiya ◽  
Miyuki Ogawa ◽  
Nagisa Matsumoto ◽  
Masashi Yamada ◽  
...  

Molecules ◽  
2019 ◽  
Vol 24 (5) ◽  
pp. 867 ◽  
Author(s):  
Hyun Park ◽  
Jong Kang ◽  
Myung Lee

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.


2004 ◽  
Vol 67 (6) ◽  
pp. 1153-1165 ◽  
Author(s):  
Tatsurou Yagami ◽  
Keiichi Ueda ◽  
Toshiyuki Sakaeda ◽  
Naohiro Itoh ◽  
Gaku Sakaguchi ◽  
...  

2015 ◽  
Vol 38 (4) ◽  
pp. 522-530 ◽  
Author(s):  
Kuan Ming Chiu ◽  
Chia Chan Wu ◽  
Ming Jiuh Wang ◽  
Ming Yi Lee ◽  
Su Jane Wang

2010 ◽  
Vol 107 (6) ◽  
pp. 958-964 ◽  
Author(s):  
Hyo Geun Kim ◽  
Mi Sun Ju ◽  
Dong-Hyun Kim ◽  
Jongki Hong ◽  
Seung-Hun Cho ◽  
...  

2012 ◽  
Vol 35 (1) ◽  
pp. 84-90 ◽  
Author(s):  
Seisuke Mimori ◽  
Yasunobu Okuma ◽  
Masayuki Kaneko ◽  
Koichi Kawada ◽  
Toru Hosoi ◽  
...  

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1368 ◽  
Author(s):  
Kkot Kim ◽  
SeonAh Lee ◽  
Inhae Kang ◽  
Jung-Hee Kim

Oxidative stress, which is induced by reactive oxygen species (ROS), causes cellular damage which contributes to the pathogenesis of neurodegenerative diseases. Momordica charantia (MC), a traditional medicinal plant, is known to have a variety of health benefits, such as antidiabetic, anti-inflammatory, and antioxidant effects. However, it is unknown whether MC has protective effects against oxidative stress-induced neuronal cell death. The aim of this study was to investigate the potential action of MC on oxidative stress induced by H2O2. First, we tested whether the pretreatment of Momordica charantia ethanol extract (MCEE) attenuates H2O2-induced cell death in human neuroblastoma SK-N-MC cells. MCEE pretreatment significantly improved cell viability and apoptosis that deteriorated by H2O2. Further, MCEE ameliorated the imbalance between intracellular ROS production and removal through the enhancement of the intracellular antioxidant system. Intriguingly, the inhibition of apoptosis was followed by the blockage of mitochondria-dependent cell death cascades and suppression of the phosphorylation of the mitogen-activated protein kinase signaling (MAPKs) pathway by MCEE. Taken together, MCEE was shown to be effective in protecting against H2O2-induced cell death through its antioxidant and anti-apoptotic properties.


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