A Newly Synthesized Rhamnoside Derivative Alleviates Alzheimer’s Amyloid-β-Induced Oxidative Stress, Mitochondrial Dysfunction, and Cell Senescence through Upregulating SIRT3

Figure 5

PL171 restored cellular SIRT3 and PGC-1α reduction induced by Aβ₄₂O. (a) Cells were treated with PL171 at different concentrations, and cell lysates were prepared and analyzed using western blotting with SIRT3 antibody. Actin was used as a loading control. (b) The quantification of relative SIRT3 protein level in (a). (c) The cell lysates in (a) were analyzed against SIRT1 antibody. (d) The quantification of relative SIRT1 protein level in (c). (e) The cell lysates in (a) were analyzed against PGC-1α antibody. (f) The quantification of relative PGC-1α protein level in (e). (g) Cells were pretreated with or without compound C (3 μM, 30 min) followed by stimulation with PL171 (30 μM, 24 h). The protein expression of AMPK phosphorylation (pAMPK), total AMPK, and SIRT3 was detected by western blotting. Actin was used as a loading control. The relative pAMPK and SIRT3 were quantified (h, i). (j) After preincubation with PL171 as indicated, cells were treated with 10 μM Aβ₄₂O for 24 h, and then cell lysates were prepared and analyzed using western blotting against SIRT3 and PGC-1α antibody. (k, l) The quantifications of relative SIRT3 and PGC-1α protein level in (j). The data are presented as , independent experiments, , , analyzed by one-way or two-way ANOVA followed by Bonferroni’s test.

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