Citicoline decreases phospholipase A2 stimulation and hydroxyl radical generation in transient cerebral ischemia

@article{Adibhatla2003CiticolineDP,
  title={Citicoline decreases phospholipase A2 stimulation and hydroxyl radical generation in transient cerebral ischemia},
  author={Rao Muralikrishna Adibhatla and James Franklin Hatcher},
  journal={Journal of Neuroscience Research},
  year={2003},
  volume={73}
}
Neuroprotection by citicoline (CDP‐choline) in transient cerebral ischemia has been demonstrated previously. Citicoline has undergone several Phase III clinical trials for stroke, and is being evaluated for treatment of Alzheimer's and Parkinson's diseases. Phospholipid degradation and generation of reactive oxygen species (ROS) are major factors causing neuronal injury in CNS trauma and neurodegenerative diseases. Oxidative metabolism of arachidonic acid (released by the action of… 

Phospholipase A2, hydroxyl radicals, and lipid peroxidation in transient cerebral ischemia.

TLDR
Results suggest that citicoline provides neuroprotection by attenuating the stimulation of PLA2, the predominant isoform in membrane and mitochondria.

Phospholipase A 2 , Hydroxyl Radicals , and Lipid Peroxidation in Transient Cerebral Ischemia

TLDR
The results suggest that citicoline provides neuroprotection by attenuating the stimulation of PLA2, the predominant isoform in membrane and mitochondria.

Reduction of lipoxidative load by secretory phospholipase A2 inhibition protects against neurovascular injury following experimental stroke in rat

TLDR
PLA2-derived oxidative products contribute to significant neurovascular damage, and treatment with sPLA2 inhibitor DEDA ameliorates secondary injury by reducing exacerbations from lipoxidative stress.

CDP-choline protects motor neurons against apoptotic changes in a model of chronic glutamate excitotoxicity in vitro.

TLDR
Results indicate that CDP-choline treatment might exert a neuroprotective effect against neuronal apoptotic changes in a model of chronic excitotoxicity in vitro.

Neuroprotection and underlying mechanisms of oxymatrine in cerebral ischemia of rats

TLDR
Oxymatrine protected the brain from damage caused by MCAO; this effect may be through down-regulation of 12/15-LOX, phospho-p38 MAPK, and cPLA2, but not through down -regulation of p38MAPK.

Thrombin induces ACSL4-dependent ferroptosis during cerebral ischemia/reperfusion

TLDR
It is reported that the serine protease, thrombin, instigates ferroptotic signaling by promoting arachidonic acid mobilization and subsequent esterification by the ferroPTotic gene, acyl-CoA synthetase long-chain family member 4 (ACSL4).

Cytidine‐5'‐Diphosphocholine Protects the Liver From Ischemia/Reperfusion Injury Preserving Mitochondrial Function and Reducing Oxidative Stress

  • C. ZazuetaM. Buelna-Chontal F. Correa
  • Biology
    Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society
  • 2018
TLDR
CDP‐choline attenuates liver damage caused by ischemia and reperfusion by reducing oxidative stress and maintaining mitochondrial function.
...

References

SHOWING 1-10 OF 75 REFERENCES

Phospholipase A2, hydroxyl radicals, and lipid peroxidation in transient cerebral ischemia.

TLDR
Results suggest that citicoline provides neuroprotection by attenuating the stimulation of PLA2, the predominant isoform in membrane and mitochondria.

Phospholipase A 2 , Hydroxyl Radicals , and Lipid Peroxidation in Transient Cerebral Ischemia

TLDR
The results suggest that citicoline provides neuroprotection by attenuating the stimulation of PLA2, the predominant isoform in membrane and mitochondria.

Effects of Citicoline on Phospholipid and Glutathione Levels in Transient Cerebral Ischemia

TLDR
The data indicated that the effects of citicoline on phospholipids occurred primarily during the first day of reperfusions, with effects on glutathione being important over the 3-day reperfusion period.

Citicoline mechanisms and clinical efficacy in cerebral ischemia

TLDR
The clinical efficacy of citicoline should be examined further in light of the recent phase III stroke clinical trials and experimental data for cerebral ischemia and several factors that might have hindered efficacy in stroke clinical Trials in the United States are evaluated.

Citicoline: neuroprotective mechanisms 
in cerebral ischemia

TLDR
The studies in transient cerebral ischemia suggest that citicoline might enhance reconstruction of PtdCho and sphingomyelin, but could act by inhibiting the destructive processes (activation of phospholipases), and a singular unifying unifying mechanism has been hypothesized.

Arachidonic Acid and Leukotriene C4: Role in Transient Cerebral Ischemia of Gerbils

TLDR
The time course of AA release, LTC4 accumulation and association with the physiological outcome during transient cerebral ischemia of gerbils is described, resulting in BBB dysfunction, edema and ultimately to neuronal death.

Cytosolic phospholipase A2 is induced in reactive glia following different forms of neurodegeneration

TLDR
It is shown that in every condition evaluated, cytosolic phospholipase A2 is present in reactive glial cells within the precise region of neuron loss, and this results suggest that cytosol phospholips A2 may prove an attractive therapeutic target for neurodegeneration.

Oxygen radicals in cerebral ischemia: the 2001 Willis lecture.

TLDR
The inhibition of AMPA receptors may be a promising approach to inhibit the production of oxygen radicals during ischemia-reperfusion of the brain.

The effects of prolonged treatment with citicoline in temporary experimental focal ischemia

CDP‐choline: Neuroprotection in transient forebrain ischemia of gerbils

TLDR
CDP‐choline significantly attenuated the blood‐brain barrier (BBB) dysfunction after ischemia with 6‐hr reperfusion, and considerably reduced the increase of AA in FFA and leukotriene C4 (LTC4) synthesis at 1 day.
...