Objective To assess the influence of aluminum maltolateAl(mal)₃ exposure on microRNA(miR)-29a and BACE1 expression in rat cortical neurons.

Methods The cerebral cortex of newborn SD rats (≤24 h old) was used for primary neuronal cultures, and 10 μmol/L of cytarabine was added on the third day. Neuron-specific class Ⅲ β-tublin was used to detect neuron purity by immunohistochemical assay. Primary neurons were exposed to different doses of Al(mal)₃ and divided into control (0 μmol/L), low dose (20 μmol/L), middle dose (40 μmol/L), and high dose (80 μmol/L) groups. After 24 h Al(mal)3 exposure, the cells were collected for determining miR-29a and BACE1 mRNA expressions by real-time fluorescence quantitative PCR, as well as BACE1 protein expression by ELISA.

Results The results of immunohistochemical assay showed the purity of neurons reaching 95%. The real-time fluorescence quantitative PCR results showed that the relative expressions of BACE1 mRNA in the control, low dose, middle dose, and high dose groups were 1.00±0.00, 1.24±0.32, 1.64±0.12, and 1.87±0.06, respectively; compared with the control group, the expression of BACE1 mRNA were increased in the middle dose group and the high dose group (P < 0.05). However, the relative expressions of miR-29a were 1.00±0.00, 0.98±0.17, 0.47±0.03, and 0.34±0.08, respectively; compared with the control group, the expressions of miR-29a were decreased in the middle dose group and the high dose group (P < 0.05). The ELISA results showed that the expressions of BACE1 in the four groups were (406.89±57.47), (419.52±49.38), (497.10±4.79), and (508.83±44.59) ng/L, respectively; compared with the control group, the levels were increased in the middle and high dose groups (P < 0.05).

Conclusion Aluminum might regulate the expression of BACE1 negatively and result in amyloid β-protein deposition through inhibiting the expression of miR-29a.