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. 2020 Mar 20;2020:9369815. doi: 10.1155/2020/9369815

Figure 4.

Figure 4

(a) Schematic representation of the RA and 9-cis RA receptors, RAR, PPAR, and RXR, and their antagonists, AGN 193109 (AGN) for RARα,β,γ and GSK 3787 (GSK) for PPARβ/δ, as well as their neuroprotective effect on Aβ-induced double-strand breaks (DSBs). (b) Effects of 5 μM all-trans-retinoic acid (RA) against Aβ-induced DSBs and of 20 μM Aβ on DSB production in the presence of the transcription inhibitor actinomycin D (Acti; 1 μg/mL) and of the translation inhibitor cycloheximide (CHX; 10 μg/mL) in SH-SY5Y cells after a 1 h treatment. The inhibitors do not interfere significantly with the effect of RA whereas they do with Aβ. Box plots of mean comet tail lengths of SH-SY5Y cells (number of cells measured: 27 < n < 50). ANOVA with Bonferroni correction: the experiment was repeated 3 times (◊p < 0.05 for 1 experiment out of 3; +p < 0.05 for 2 experiments out of 3; ∗p < 0.05 for 3 experiments out of 3). (c) Box plots of mean comet tail lengths of SH-SY5Y cells (31 < n < 53) following a 1 h treatment with RA, 9-cis RA (5 μM), and/or Aβ in the presence of AGN (50 μM) or not. (d) Box plots of mean comet tail lengths of SH-SY5Y cells (36 < n < 50) following a 30 min treatment with Aβ, RA, AGN, and GSK (10−5 M) and a combination of these factors. (e) Box plots of mean comet tail lengths of SH-SY5Y cells (31 < n < 34) following a 30 min treatment with RA, AGN, and/or GSK, and after a washing step, a second 30 min treatment with Aβ or not. (c–e) ANOVA with Bonferroni correction: ∗p < 0.05. ø = without treatment.