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== Effects on ALS == | == Effects on ALS == | ||
| − | In rat brain cortical motoneuron primary culture, resveratrol '''protects against neurotoxic effects and antagonizes the [Ca(+2)](c) elevation''' produced by ALS/CSF. However, riluzole does not afford protection and antagonizes the resveratrol-elicited neuroprotective effects. {{#pmid:21983205|yanez2011}} | + | In rat brain cortical motoneuron primary culture, resveratrol '''protects against neurotoxic effects and antagonizes the [Ca(+2)](c) elevation''' produced by ALS/CSF. However, riluzole does not afford protection and antagonizes the resveratrol-elicited neuroprotective effects. {{#pmid:21983205|yanez2011}} {{#pmidː21983205|yanez2011}} |
| − | ''Our results indicate that resveratrol potently '''reduced LPS-induced PGE2 synthesis and the formation of 8-iso-PGF2 alpha, a measure of free radical production'''. Interestingly, resveratrol dose-dependently '''reduced the expression (mRNA and protein) of mPGES-1, which is a key enzyme responsible for the synthesis of PGE2 by activated microglia''', whereas resveratrol did not affect the expression of COX-2. Resveratrol is therefore the '''first known inhibitor which specifically prevents mPGES-1 expression without affecting COX-2 levels'''. Another important observation of the present study is that other COX-1 selective inhibitors (SC-560 and Valeroyl Salicylate) potently reduced PGE2 and 8-iso-PGF2 alpha production by LPS-activated microglia. These findings suggest that the naturally occurring polyphenol resveratrol is '''able to reduce microglial activation''', an effect that might help to explain its neuroprotective effects in several in vivo models of brain injury.'' {{# | + | ''Our results indicate that resveratrol potently '''reduced LPS-induced PGE2 synthesis and the formation of 8-iso-PGF2 alpha, a measure of free radical production'''. Interestingly, resveratrol dose-dependently '''reduced the expression (mRNA and protein) of mPGES-1, which is a key enzyme responsible for the synthesis of PGE2 by activated microglia''', whereas resveratrol did not affect the expression of COX-2. Resveratrol is therefore the '''first known inhibitor which specifically prevents mPGES-1 expression without affecting COX-2 levels'''. Another important observation of the present study is that other COX-1 selective inhibitors (SC-560 and Valeroyl Salicylate) potently reduced PGE2 and 8-iso-PGF2 alpha production by LPS-activated microglia. These findings suggest that the naturally occurring polyphenol resveratrol is '''able to reduce microglial activation''', an effect that might help to explain its neuroprotective effects in several in vivo models of brain injury.'' {{#pmidː17927823|candelario2007}} |
''Here, we report that a human homologue of SIR2, SIRT1, is upregulated in mouse models for AD, ALS and in primary neurons challenged with neurotoxic insults. '''In cell-based models for AD/tauopathies and ALS, SIRT1 and resveratrol, a SIRT1-activating molecule, both promote neuronal survival'''. In the inducible p25 transgenic mouse, a model of AD and tauopathies, resveratrol reduced neurodegeneration in the hippocampus, prevented learning impairment, and decreased the acetylation of the known SIRT1 substrates PGC-1alpha and p53.'' {{#pmid:17581637|kim2007}} | ''Here, we report that a human homologue of SIR2, SIRT1, is upregulated in mouse models for AD, ALS and in primary neurons challenged with neurotoxic insults. '''In cell-based models for AD/tauopathies and ALS, SIRT1 and resveratrol, a SIRT1-activating molecule, both promote neuronal survival'''. In the inducible p25 transgenic mouse, a model of AD and tauopathies, resveratrol reduced neurodegeneration in the hippocampus, prevented learning impairment, and decreased the acetylation of the known SIRT1 substrates PGC-1alpha and p53.'' {{#pmid:17581637|kim2007}} | ||
