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. 2017 Sep 12;7:11408. doi: 10.1038/s41598-017-11628-9

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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SOD-3 was required for DXN inhibiting Aβ toxicity. (A) sod-3 expression was up-regulated after 15 mg/mL DXN treatment, and worms were treated with 20 mM juglone as positive control. The scale bar was 40 μm. (B) Quantification of sod-3 expression. (C) 15 mg/mL DXN inhibited the expression of Phsp-16.2::GFP induced by 40 μM juglone, and worms treated with 20 mM juglone were used as positive control. The scale bar was 25 μm. (D) Quantification of the expression of hsp-16.2. In (A–D), data are the average of three replicates with about 90 worms in each group. There is significant difference among these groups when symbols are different (P < 0.05). (E) The effects of sod-3 RNAi and hsp16.2 RNAi on DXN inhibiting worm paralysis induced by Aβ_1-42 over-expression. Data are the average of three replicates with about 120–180 worms in each group. ***Indicated that there was significant difference between treatment groups and control group at P < 0.001.