Conclusion
miR-132 could downregulate the expression of HMGA2 and promote the expression of the PI3K/AKT pathway, so as to achieve a protective effect on brain in AD mice.
Methods
The mice were divided into 7 groups: the normal group, the model group (AD model mice), the NC group (AD mice injected with negative control (NC) vector), the miR-132 mimic group (AD mice injected with miR-132 mimics), the miR-132 inhibitor group (AD mice injected with miR-132 inhibitor), the si-HMGA2 group (AD mice injected with HMGA2 silencing vector), and the miR-132 inhibitor + si-HMGA2 group (model mice treated with miR-132 inhibitor and si-HMGA2). Y-maze experiment and related molecular biology experiments were performed.
Objective
To explore the role and of miR-132, HMGA2 and PI3K/AKT pathway in mice with Alzheimer's disease (AD).
Results
The double-luciferase reporter assay verified that miR-132 could target and inhibit the expression of HMGA2A. Compared with the NC group, model mice had decreased learning and memory ability, reduced miR-132, p-PI3K/PI3K, p-AKT/AKT, AQP4 expression as well as GFAP GSH-Px, SOD, ATP, and T-AOC levels, but increased expression of HMGA2 and the levels of TNF-α, IL-6, NO, IL-1β, MAO, and MDA (P<0.017). Up-regulation of miR-132 or silencing HMGA2 could partly reverse the changes, but inhibition of miR-132 would exaggerate the brain injury and these molecular changes (P<0.017). The combination uses of si-HMGA2 and miR-132 inhibitor could reverse the changes caused by miR-132 inhibitor (P<0.017).