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. 2015 Feb 18;20(3):3496–3514. doi: 10.3390/molecules20033496

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© 2015 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/4.0/).

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Neferine reduces the toxicity of mutant huntingtin in cells. (A) PC-12 cells transfected with huntingtin with 74 CAG repeats for 16 h were treated with neferine for a further 24 h. Cell viability was then measured by the MTT assay or (B) by counting the number of viable cells after treatments. A significantly higher percentage of cell viability was detected after neferine treatments. (C) Wild-type Atg7 and Atg7-deficient MEF cells transfected with huntingtin with 74 CAG repeats (EGFP-HTT 74) for 6 h were treated with neferine for a further 48 h. A significant lower percentage of cells with positive propidium iodide staining (cell death) and GFP signals was detected in wild-type Atg7 cells after neferine treatments. Data from the bar chart represent the means ± SD of three independent experiments. * p < 0.05; ** p < 0.01; *** p < 0.001.

Neferine reduces the toxicity of mutant huntingtin in cells. (A) PC-12 cells transfected with huntingtin with 74 CAG repeats for 16 h were treated with neferine for a further 24 h. Cell viability was then measured by the MTT assay or (B) by counting the number of viable cells after treatments. A significantly higher percentage of cell viability was detected after neferine treatments. (C) Wild-type Atg7 and Atg7-deficient MEF cells transfected with huntingtin with 74 CAG repeats (EGFP-HTT 74) for 6 h were treated with neferine for a further 48 h. A significant lower percentage of cells with positive propidium iodide staining (cell death) and GFP signals was detected in wild-type Atg7 cells after neferine treatments. Data from the bar chart represent the means ± SD of three independent experiments. * p < 0.05; ** p < 0.01; *** p < 0.001.

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