ABSTRACT
We studied the effects of endocannabinoid anandamide and its cyclooxygenase derivative prostamide E2 on cultured cerebellar granular cells and C6 glioma cells from rats. Prostamide E2 prevented apoptosis in cerebellar neurons induced by potassium deprivation of cultures, while anandamide had no neuroprotective properties. Prostamide E2 did not modulate the survival rate of glioma cells, while anandamide produced a cytotoxic effect. Our results indicate that cyclooxygenase transformation of anandamide is followed by the loss of antitumor activity of this agent. By contrast, prostamide E2 exhibited strong neuroprotective properties.
Subject(s)
Arachidonic Acids/metabolism , Dinoprostone/analogs & derivatives , Neurons/drug effects , Neuroprotective Agents/pharmacology , Polyunsaturated Alkamides/metabolism , Potassium/pharmacology , Animals , Apoptosis/drug effects , Arachidonic Acids/pharmacology , Biotransformation , Cell Survival/drug effects , Cells, Cultured , Cerebellum/cytology , Cerebellum/drug effects , Cerebellum/metabolism , Dinoprostone/metabolism , Dinoprostone/pharmacology , Dose-Response Relationship, Drug , Endocannabinoids , Glioma/metabolism , Glioma/pathology , Neurons/cytology , Neurons/metabolism , Neuroprotective Agents/metabolism , Polyunsaturated Alkamides/pharmacology , Potassium/metabolism , Potassium Deficiency/metabolism , Primary Cell Culture , Prostaglandin-Endoperoxide Synthases/metabolism , RatsABSTRACT
N-Docosahexaenoyl dopamine exhibited antioxidant activity in the test with a stable oxygen radical galvinoxyl. This compound produced a dose-dependent protective effect on cultured granular cells from rat cerebellum under conditions of oxidative stress. N-Docosahexaenoyl dopamine decelerated the development of symptoms of Parkinson's disease in mice receiving neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.
