MiR-130a-3p Has Protective Effects in Alzheimer's Disease via Targeting DAPK1.

The present study investigated the role and potential mechanisms of miR-130a-3p in AD. SH-SY5Y cells were treated with Aß 1-42 to construct AD cell models. APP/PS1 mice were used for the animal experiments. MiR-130a-3p was downregulated in Aß-induced SH-SY5Y cells. Overexpression of miR-130a-3p attenuates Aß induced SH-SY5Y cell apoptosis. Low miR-130a-3p expression was detected in the hippocampus tissues of AD mice. The Morris water maze (MWM) results indicated that miR-130a-3p upregulation reduced the escape latency time and increased the time of AD mice spent in the target quadrant. DAPK1 was the target gene of miR-130a-3p. High DAPK1 mRNA level was detected in Aß treated PC 12 cells and in the hippocampus tissues of AD mice. It was concluded that overexpression of miR-130a-3p may attenuate Aß-induced neurotoxicity and improve the cognitive function of AD mice via targeting DAPK1.

CGA restrains the apoptosis of Aß25-35-induced hippocampal neurons.

Background: Chlorogenic acid (CGA) has anti-oxidant and anti-inflammatory effects, but the study on its role in Alzheimer's disease (AD) models remains rare. Here, the effects of CGA on ß-amyloid protein (Aß)-induced cell models were investigated, aiming to provide a direction for Aß-induced AD.Material and methods: Hippocampal neurons were separated from newborn Sprague-Dawley (SD) rats and identified by immumofluorescence method. Hippocampal neurons were processed with Aß25-35 after pre-treatment CGA. MTT assay was used for detecting viability of treated cells. The activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA) and lactate dehydrogenase (LDH) of treated hippocampal neurons were determined by corresponding kits. Flow cytometry analysis assessed the apoptosis and mitochondrial membrane potential (MMP) in hippocampal neurons after treatment. The expressions of proteins related to apoptosis and endoplasmic reticulum stress (ERS) were measured by western blot (WB) analysis.Results: Immumofluorescence method showed that the Aß25-35 induction models were successfully constructed. CGA increased the viability and decreased the apoptosis rate of Aß25-35-induced hippocampal neurons. Decreasing activities of LDH and MDA, and raised contents of SOD and GSH-Px were appeared in Aß25-35-induced cells that pre-treated with CGA. Moreover, CGA also enhanced MMP intensity of hippocampal neurons induced by Aß25-35. In WB analysis, CGA reversed the promoting effect of Aß25-35 on the expressions of proteins related to pro-ERS and pro-apoptosis.Conclusion: CGA restrained the apoptosis of Aß25-35-induced hippocampal neurons via improving the anti-oxidant capacity, mitochondrial injury and ERS state of cells, which may provide a direction for AD.