miR-103a-3p/RCANl 通路 在铝致大鼠学习记忆损害的作用.

Objective To explore the role of miR -103a-3p/regulator of calcineurinl (RCAN1) pathway in maltol aluminum induced memory impairment in rats. Methods In total 32 male SD rats were randomly divided into control group (0 (xmol/kg), low dose aluminum exposure group (10 (xmol/kg), medium dose aluminum exposure group (20 |Jimol/kg), and high dose aluminum exposure group (40 (xmol/kg), with 8 rats in each group. The rats in the control group were intraperitoneally injected with 0.9% normal saline, and the aluminum group was injected with maltol aluminum solution of corresponding concentration every other day for 3 months. After exposure, the learning and memory ability of rats was assessed by water maze test, the gene expression of miR-103a-3p and RCAN1 was detected by real-time fluorescence quantitative PCR, and the relative expressions of RCAN1, glycogen synthesis kinase-3 0 (GSK-3 |3), and phosphorylated tau protein in hippocampus were detected by Western blotting. Results The escape latency in the aluminum exposed group was higher than that in the control group in the first five days, and the residence time in the target quadrant and the number of times crossing the platform in the aluminum exposed group were lower than those in the control group (P<0.05) on the sixth day of spatial exploration. Compared with the control group, the expression level of miR103a-3p gene in hippocampus of aluminum exposed group decreased (P< 0.001), while the expression level of RCAN1 gene increased (P<0.001). Compared with the control group, the expression of RCAN1, GSK3 [3, and p-tau (ser396) protein in hippocampus of aluminum exposed group increased (P<0.001). Conclusion MiR-103a-3p/RCANl pathway is involved in the regulation of learning and memory impairment induced by aluminum. [ABSTRACT FROM AUTHOR]