Electrophoretic studies on the phosphorylation of stathmin and mitogen-activated protein kinases in neuronal cell death induced by oxidized very-low-density lipoprotein with apolipoprotein E

2002 ◽  
Vol 23 (7-8) ◽  
pp. 998-1004 ◽  
Author(s):  
Hiroshi Yamashita ◽  
Kazuyuki Nakamura ◽  
Hirofumi Arai ◽  
Hiroko Furumoto ◽  
Masanori Fujimoto ◽  
...  
Keyword(s):  
Cell Death ◽  
Protein Kinases ◽  
Low Density Lipoprotein ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Mitogen Activated Protein Kinases ◽  
Mitogen Activated Protein

scholarly journals Neuroprotective Effects of Tetrahydrocurcumin against Glutamate-Induced Oxidative Stress in Hippocampal HT22 Cells

Molecules ◽  
2019 ◽  
Vol 25 (1) ◽  
pp. 144 ◽  
Author(s):  
Chang-Hyun Park ◽  
Ji Hoon Song ◽  
Su-Nam Kim ◽  
Ji Hwan Lee ◽  
Hae-Jeung Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Protein Kinases ◽  
Apoptotic Cell ◽  
Curcuma Longa ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Ht22 Cells ◽  
Mitogen Activated Protein Kinases ◽  
Mitogen Activated Protein

In the central nervous system, glutamate is a major excitable neurotransmitter responsible for many cellular functions. However, excessive levels of glutamate induce neuronal cell death via oxidative stress during acute brain injuries as well as chronic neurodegenerative diseases. The present study was conducted to examine the effect of tetrahydrocurcumin (THC), a major secondary metabolite of curcumin, and its possible mechanism against glutamate-induced cell death. We prepared THC using curcumin isolated from Curcuma longa (turmeric) and demonstrated the protective effect of THC against glutamate-induced oxidative stress in HT22 cells. THC abrogated glutamate-induced HT22 cell death and showed a strong antioxidant effect. THC also significantly reduced intracellular calcium ion increased by glutamate. Additionally, THC significantly reduced the accumulation of intracellular oxidative stress induced by glutamate. Furthermore, THC significantly diminished apoptotic cell death indicated by annexin V-positive in HT22 cells. Western blot analysis indicated that the phosphorylation of mitogen-activated protein kinases including c-Jun N-terminal kinase, extracellular signal-related kinases 1/2, and p38 by glutamate was significantly diminished by treatment with THC. In conclusion, THC is a potent neuroprotectant against glutamate-induced neuronal cell death by inhibiting the accumulation of oxidative stress and phosphorylation of mitogen-activated protein kinases.

Phenolic antioxidants attenuate neuronal cell death following uptake of oxidized low-density lipoprotein

2000 ◽  
Vol 29 (12) ◽  
pp. 1222-1233 ◽  
Author(s):  
Hagen Schroeter ◽  
Robert J Williams ◽  
Rubeta Matin ◽  
Leslie Iversen ◽  
Catherine A Rice-Evans
Keyword(s):  
Cell Death ◽  
Low Density Lipoprotein ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Density Lipoprotein ◽  
Phenolic Antioxidants ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein

Studies on the Thromboplastic Effect of Human Plasma Lipoproteins

1976 ◽  
Vol 35 (01) ◽  
pp. 178-185 ◽  
Author(s):  
Helena Sandberg ◽  
Lars-Olov Andersson
Keyword(s):  
High Density Lipoprotein ◽  
Human Plasma ◽  
Platelet Rich Plasma ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Plasma Lipoproteins ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Free Plasma ◽  
Good Agreement

SummaryHuman plasma lipoprotein fractions were prepared by flotation in the ultracentrifuge. Addition of these fractions to platelet-rich, platelet-poor and platelet-free plasma affected the partial thromboplastin and Stypven clotting times to various degrees. Addition of high density lipoprotein (HDL) to platelet-poor and platelet-free plasma shortened both the partial thromboplastin and the Stypven time, whereas addition of low density lipoprotein and very low density lipoprotein (LDL + VLDL) fractions only shortened the Stypven time. The additions had little or no effect in platelet-rich plasma.Experiments involving the addition of anti-HDL antibodies to plasmas with different platelet contents and measuring of clotting times produced results that were in good agreement with those noted when lipoprotein was added. The relation between structure and the clot-promoting activity of various phospholipid components is discussed.

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