This article explores the mechanism of miR-194 on the proliferation and apoptosis of Aβ1-42-transduced hippocampal neurons. Aβ1-42-transduced hippocampal neuron model was established by inducing hippocampal neurons with Aβ1-42. MTT assay and flow cytometry were used to detect the viability and apoptosis of hippocampal neurons, respectively. qRT-PCR was used to detect changes in miR-194 and Nrn1 expression after Aβ1-42 induction. Aβ1-42-transduced hippocampal neurons were transfected with miR-194 mimics and/or Nrn1 overexpression vectors. Their viability and neurite length were detected by MTT assay and immunofluorescence, respectively. Western blot was used to detect protein expression. Aβ1-42 inhibited Aβ1-42-transduced hippocampal neuron activity and promoted their apoptosis in a dose-dependent manner. miR-194 was upregulated and Nrn1 was downregulated in Aβ1-42-transduced hippocampal neurons (p < 0.05). Compared with the model group, Aβ1-42-transduced hippocampal neurons of the miR-194 mimic group had much lower activity, average longest neurite length, Nrn1, p-AkT, and Bcl-2 protein expression and had much higher Bax, Caspase-3, and Cleaved Caspase-3 protein expression. Compared with the model group, Aβ1-42-transduced hippocampal neurons of the LV-Nrn1 group had much higher activity, average longest neurite length, Nrn1, p-AkT, and Bcl-2 protein expression and had much lower Bax, Caspase-3, and Cleaved Caspase-3 protein expression. Nrn1 is a target gene of miR-194. miR-194 inhibited apoptosis of Aβ1-42-transduced hippocampal neurons by inhibiting Nrn1 and decreasing PI3K/AkT signaling pathway activity.
Keywords: Alzheimer’s disease; Nrn1; PI3K/AkT signaling pathway; apoptosis; hippocampal neurons; miR-194; proliferation.