Abstract：Objective To explore the protective effect and possible mechanism of β-hydroxybutyrate (BHB) on SH-SY5Y cells exposed to β-amyloidpeptide (Aβ), and to provide a theoretical basis for prevention and treatment of Alzheimer’s disease. Methods SH-SY5Y cells cultured in vitro were divided into 4 groups. Cells in the BHB group and the BHB-intervened group were pretreated with BHB (final concentration of 5 mM) for 3 h, then cells in the Aβ group and the BHB-intervened group were treated with Aβ (final concentration of 20 μM), and sham-treated cells were used as the control group. All the cells were collected at 24 h after the treatment. The relative expression of TrkA, HDAC1 and HDAC3 mRNA and protein in the cells of each group were detected by qRT-PCR and Western Blot respectively. In addition, the relative expression of TrkA mRNA and protein was analyzed in cells after silencing HDAC1/3 with siRNA. Results Compared with the control group, the relative expression of TrkA mRNA and protein in cells of the BHB group increased significantly (P<0.05), while the relative expression of HDAC1 and HDAC3 mRNA and protein declined obviously (P<0.05). Compared with the control group, the relative expression of TrkA mRNA and protein in cells of the Aβ group reduced remarkably (P<0.01), while the relative expression of HDAC1 and HDAC3 mRNA and protein increased significantly (P<0.01). Compared with the Aβ group, the relative expression of TrkA mRNA and protein in cells of the BHB-intervened group ascended significantly (P<0.01), while the relative expression of HDAC1 and HDAC3 mRNA and protein descended obviously (P<0.01). In HDAC1 or 3-silenced cells, the relative expression of TrkA mRNA and protein increased distinctly (P<0.05). Conclusions BHB may up-regulate the TrkA expression via inhibiting HDAC1/3 in SH-SY5Y cells exposed to Aβ.
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2018, Vol. 25 
