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Abstract
It has recently been reported that methyl-beta-cyclodextrin-solubilized cholesterol
protects PC12 cells from amyloid beta protein (Abeta) toxicity. To ask if this is
the case in brain neurons, we investigated its effect in primary cultured rat hippocampal
neurons. In basal culture conditions with no addition of Abeta, methyl-beta-cyclodextrin-solubilized
cholesterol at concentrations of 30-100 microM was toxic to neurons, but at concentrations
of 1-10 microM promoted neuronal survival. Methyl-beta-cyclodextrin-solubilized cholesterol
at 1-10 microM was also effective in protecting neurons from toxicity of 20 microM
Abeta. However, these effects were all mimicked by methyl-beta-cyclodextrin alone,
but not by cholesterol solubilized by dimethylsulfoxide or ethanol. The effects of
methyl-beta-cyclodextrin-solubilized cholesterol on neuronal survival and Abeta toxicity
are probably attributed to the action of methyl-beta-cyclodextrin, but not cholesterol.
Alternatively, we found that methyl-beta-cyclodextrin-solubilized cholesterol at lower
concentrations ( > 10 nM) inhibited cellular reduction of 3-(4,5-dimethylthiazol-2-yl)-2.5-diphenyltetrazolium
bromide (MTT) by promoting the exocytosis of MTT formazan. This effect was shared
by dimethylsulfoxide- or ethanol-solubilized cholesterol, but not by methyl-beta-cyclodextrin,
supporting that it is attributed to the action of cholesterol. These results suggest
that cholesterol does not protect neurons from Abeta toxicity, or rather inhibits
cellular MTT reduction in a similar manner to Abeta.