Electroacupuncture Reduces Scopolamine-Induced Amnesia Via Mediating the miR-210/SIN3A and miR-183/SIN3A Signaling Pathway
Background The expression of SIN3A is closely correlated with EA treatment efficacy of SIA, but its underlying mechanisms remain to be further explored.
Methods Quantitative real-time PCR was performed to analyze the expression of candidate miRNAs and SIN3A mRNA in a rat model of SIA. Western blot was carried out to evaluate the differential expression of SIN3A proteins under distinct circumstances. Luciferase assay was used to explore the inhibitory role of certain miRNAs in SIN3A expression. NOR test was performed to assess the memorial ability of SIA rats undergoing EA treatment. Immunohistochemistry was carried out to evaluate the expression of SIN3A in the hippocampus of SIA rats.
Results Rno-miR-183-5p, rno-miR-34c-3p and rno-miR-210-3p were significantly up-regulated in SIA rats treated with EA. In addition, rno-miR-183-5p and rno-miR-210-3p exerted an inhibitory effect on SIN3A expression. EA treatment of SIA rats effectively restored the normal expression of rno-miR-183-5p, rno-miR-210-3p and SIN3A. The NOR test also confirmed the effect of EA treatment on the improvement of memory in SIA rats.
Conclusion In this study, an animal model of SIA was treated with EA to investigate its therapeutic effect. Moreover, our work presented solid evidence on the regulatory pathway of miR-183/SIN3A and miR-210/SIN3A in the pathogenesis of SIA.
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On 12 Nov, 2020
On 20 Oct, 2020
On 20 Oct, 2020
On 19 Oct, 2020
On 19 Oct, 2020
On 05 Oct, 2020
On 05 Oct, 2020
On 04 Oct, 2020
On 04 Oct, 2020
On 15 Sep, 2020
On 14 Sep, 2020
On 14 Sep, 2020
On 24 Aug, 2020
Received 22 Aug, 2020
On 03 Aug, 2020
Invitations sent on 03 Aug, 2020
On 03 Aug, 2020
On 02 Aug, 2020
On 02 Aug, 2020
Posted 28 May, 2020
On 28 Jun, 2020
Received 27 Jun, 2020
Received 24 Jun, 2020
On 13 Jun, 2020
On 10 Jun, 2020
Invitations sent on 09 Jun, 2020
On 02 Jun, 2020
On 01 Jun, 2020
On 26 May, 2020
On 22 May, 2020
Electroacupuncture Reduces Scopolamine-Induced Amnesia Via Mediating the miR-210/SIN3A and miR-183/SIN3A Signaling Pathway
On 12 Nov, 2020
On 20 Oct, 2020
On 20 Oct, 2020
On 19 Oct, 2020
On 19 Oct, 2020
On 05 Oct, 2020
On 05 Oct, 2020
On 04 Oct, 2020
On 04 Oct, 2020
On 15 Sep, 2020
On 14 Sep, 2020
On 14 Sep, 2020
On 24 Aug, 2020
Received 22 Aug, 2020
On 03 Aug, 2020
Invitations sent on 03 Aug, 2020
On 03 Aug, 2020
On 02 Aug, 2020
On 02 Aug, 2020
Posted 28 May, 2020
On 28 Jun, 2020
Received 27 Jun, 2020
Received 24 Jun, 2020
On 13 Jun, 2020
On 10 Jun, 2020
Invitations sent on 09 Jun, 2020
On 02 Jun, 2020
On 01 Jun, 2020
On 26 May, 2020
On 22 May, 2020
Background The expression of SIN3A is closely correlated with EA treatment efficacy of SIA, but its underlying mechanisms remain to be further explored.
Methods Quantitative real-time PCR was performed to analyze the expression of candidate miRNAs and SIN3A mRNA in a rat model of SIA. Western blot was carried out to evaluate the differential expression of SIN3A proteins under distinct circumstances. Luciferase assay was used to explore the inhibitory role of certain miRNAs in SIN3A expression. NOR test was performed to assess the memorial ability of SIA rats undergoing EA treatment. Immunohistochemistry was carried out to evaluate the expression of SIN3A in the hippocampus of SIA rats.
Results Rno-miR-183-5p, rno-miR-34c-3p and rno-miR-210-3p were significantly up-regulated in SIA rats treated with EA. In addition, rno-miR-183-5p and rno-miR-210-3p exerted an inhibitory effect on SIN3A expression. EA treatment of SIA rats effectively restored the normal expression of rno-miR-183-5p, rno-miR-210-3p and SIN3A. The NOR test also confirmed the effect of EA treatment on the improvement of memory in SIA rats.
Conclusion In this study, an animal model of SIA was treated with EA to investigate its therapeutic effect. Moreover, our work presented solid evidence on the regulatory pathway of miR-183/SIN3A and miR-210/SIN3A in the pathogenesis of SIA.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
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Figure 8