Acetoacetate protects neuronal cells from oxidative glutamate toxicity

2006 ◽  
Vol 83 (4) ◽  
pp. 702-709 ◽  
Author(s):  
Hae Sook Noh ◽  
Young-Sool Hah ◽  
Rashidova Nilufar ◽  
Jaehee Han ◽  
Jae-Hwan Bong ◽  
...  
Keyword(s):  
Neuronal Cells ◽  
Glutamate Toxicity

Glutamate Toxicity in the Lung and Neuronal Cells: Prevention or Attenuation by VIP and PACAP

1998 ◽  
Vol 865 (1 VIP, PACAP, A) ◽  
pp. 226-237 ◽  
Author(s):  
S. I. SAID ◽  
K. DICKMAN ◽  
R. D. DEY ◽  
A. BANDYOPADHYAY ◽  
P. STEFANIS ◽  
...  
Keyword(s):  
Neuronal Cells ◽  
Glutamate Toxicity

scholarly journals Proteasome inhibition protects HT22 neuronal cells from oxidative glutamate toxicity

2005 ◽  
Vol 92 (4) ◽  
pp. 824-830 ◽  
Author(s):  
Klaus van Leyen ◽  
Ambreena Siddiq ◽  
Rajiv R. Ratan ◽  
Eng H. Lo
Keyword(s):  
Neuronal Cells ◽  
Proteasome Inhibition ◽  
Glutamate Toxicity

scholarly journals Protection of SH-SY5Y Neuronal Cells from Glutamate-Induced Apoptosis by 3,6′-Disinapoyl Sucrose, a Bioactive Compound Isolated from Radix Polygala

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Yuan Hu ◽  
Jie Li ◽  
Ping Liu ◽  
Xu Chen ◽  
Dai-Hong Guo ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Cell Viability ◽  
Mtt Assay ◽  
Neuronal Cells ◽  
Bioactive Compound ◽  
Glutamate Toxicity ◽  
Flow Cytometry Assay ◽  
Neuroprotective Effects ◽  
Induced Apoptosis ◽  
Proapoptotic Gene

The neuroprotective effects of 3,6′-disinapoyl sucrose (DISS) from Radix Polygala against glutamate-induced SH-SY5Y neuronal cells injury were evaluated in the present study. SH-SY5Y neuronal cells were pretreated with glutamate (8 mM) for 30 min followed by cotreatment with DISS for 12 h. Cell viability was determined by (3,4,5-dimethylthiazol-2-yl)-2,5-diphenylte-trazolium bromide (MTT) assay, and apoptosis was confirmed by cell morphology and flow cytometry assay, evaluated with propidium iodide dye. Treatment with DISS (0.6, 6, and 60 μmol/L) increased cell viability dose dependently, inhibited LDH release, and attenuated apoptosis. The mechanisms by which DISS protected neuron cells from glutamate-induced excitotoxicity included the downregulation of proapoptotic gene Bax and the upregulation of antiapoptotic gene Bcl-2. The present findings indicated that DISS exerts neuroprotective effects against glutamate toxicity, which might be of importance and contribute to its clinical efficacy for the treatment of neurodegenerative diseases.

Protection of HT22 neuronal cells against glutamate toxicity mediated by the antioxidant activity of Pueraria candollei var. mirifica extracts

2010 ◽  
Vol 65 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Apirada Sucontphunt ◽  
Wanchai De-Eknamkul ◽  
Ubonthip Nimmannit ◽  
S. Dan Dimitrijevich ◽  
Robert W. Gracy
Keyword(s):  
Antioxidant Activity ◽  
Neuronal Cells ◽  
Glutamate Toxicity ◽  
Pueraria Candollei

Cytoprotective Effect of Tocotrienol-Rich Fraction and α-Tocopherol Vitamin E Isoforms Against Glutamate-Induced Cell Death in Neuronal Cells

2014 ◽  
Vol 84 (3-4) ◽  
pp. 0140-0151 ◽  
Author(s):  
Thilaga Rati Selvaraju ◽  
Huzwah Khaza’ai ◽  
Sharmili Vidyadaran ◽  
Mohd Sokhini Abd Mutalib ◽  
Vasudevan Ramachandran ◽  
...  
Keyword(s):  
Vitamin E ◽  
Cell Viability ◽  
Neuronal Cells ◽  
Positive Control ◽  
Post Treatment ◽  
Mitochondrial Activity ◽  
Before And After ◽  
Pre Treatment ◽  
Tocotrienol Rich Fraction ◽  
Major Mediator

Glutamate is the major mediator of excitatory signals in the mammalian central nervous system. Extreme amounts of glutamate in the extracellular spaces can lead to numerous neurodegenerative diseases. We aimed to clarify the potential of the following vitamin E isomers, tocotrienol-rich fraction (TRF) and α-tocopherol (α-TCP), as potent neuroprotective agents against glutamate-induced injury in neuronal SK-N-SH cells. Cells were treated before and after glutamate injury (pre- and post-treatment, respectively) with 100 - 300 ng/ml TRF/α-TCP. Exposure to 120 mM glutamate significantly reduced cell viability to 76 % and 79 % in the pre- and post-treatment studies, respectively; however, pre- and post-treatment with TRF/α-TCP attenuated the cytotoxic effect of glutamate. Compared to the positive control (glutamate-injured cells not treated with TRF/α-TCP), pre-treatment with 100, 200, and 300 ng/ml TRF significantly improved cell viability following glutamate injury to 95.2 %, 95.0 %, and 95.6 %, respectively (p < 0.05).The isomers not only conferred neuroprotection by enhancing mitochondrial activity and depleting free radical production, but also increased cell viability and recovery upon glutamate insult. Our results suggest that vitamin E has potent antioxidant potential for protecting against glutamate injury and recovering glutamate-injured neuronal cells. Our findings also indicate that both TRF and α-TCP could play key roles as anti-apoptotic agents with neuroprotective properties.

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