کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2590400 | 1131740 | 2008 | 8 صفحه PDF | دانلود رایگان |
Galantamine, an acetylcholinesterase inhibitor used to enhance memory in AD patients by acetylcholinesterase inhibition, has been tested for its protective properties on an in vitro model of H2O2-induced oxidative stress. SK–N–SH cells treated with H2O2 for 2 h showed an increase in ROS production (54%) and in NO production (52%) together with a marked reduction of the mitochondrial membrane potential (19%). These features, typical of the oxidative injury that accompanies AD, were partly recovered by galantamine. Galantamine reduced the release of reactive oxygen species (up to 50%) and prevented loss in mitochondrial activity. When SK–N–SH cells were treated with H2O2 for 24 h, nitrite generation was increased by twice compared with 2 h. Galantamine treatment resulted in a significant inhibition of H2O2-induced nitrite generation whatever the concentration tested with a return to control values. Galantamine also concentration-dependently inhibited AChE activity (28–88%) in H2O2–SK–N–SH cells after 24 h. This drug, which facilitates cholinergic neurotransmission, is also neuroprotective by lowering oxidative injury. Our study provides a better understanding of the mechanisms of protection of this acetylcholinesterase inhibitor which also has antioxidative properties.
Journal: NeuroToxicology - Volume 29, Issue 2, March 2008, Pages 270–277