ABSTRACT
To observe the effect of puerarin on learning and memory function and tau phosphorylation in APP/PS1 transgenic mice, drugs were administered to 3-month old APP/PS1 transgenic mice. Learning and memory function of mice were assessed by Morris water maze test 3 months after treatment. Animals were decapitated after behavioral test. The levels of Aβ were detected by ELISA, the expression of protein [tau, phosphorylated tau, GSK3β and p-GSK3β(Ser9)] were assessed by Western blot. Morris water maze test showed that the escape latency of APP/PS1 double transgenic mice was significantly longer than that of the normal control group, and the residence time of the original quadrant was significantly shorter. The escape latency of puerarin group was significantly shorter and the residence time of the original quadrant was prolonged compared with the model group. Compared with the normal control group, the levels of Aβ in the cortex of APP/PS1 transgenic mice were increased, the expression of phosphorylated tau was significantly increased, and the expression of phosphorylated GSK3β(Ser9) protein was decreased. Treatment with puerarin, the latency of APP/PS1 transgenic mice was significantly reduced, the level of Aβ was decreased, the expression of phosphorylated tau was significantly decreased, and the expression of phosphorylated GSK3β(Ser9) protein was increased. Puerarin improves the learning and memory impairment by reducing the formation of Aβ, activating the GSK3β signaling pathway, inhibiting the phosphorylation of tau in APP/PS1 double transgenic mice.
ABSTRACT
<p><b>OBJECTIVE</b>To establish a model of smooth muscle cells differentiated from bone mesenchymal stem cells (BMSC-SMCs) in vitro and explore the relationship between scavenger receptors A (SR-A) and caveolin-1.</p><p><b>METHODS</b>BMSCs were isolated from the femoral bone of SD rats by adherent culture. After treatment of the BMSC-SMCs with 80 mg/L ox-LDL for 72 h, Western blotting was performed to detect the expression of scavenger receptor SR-A, cell cholesterol transport protein ATP-binding cassette transporter Al (ABCA1) and caveolin-1.</p><p><b>RESULTS</b>BMCS-SMCs became foam cells after treatment with ox-LDL. BMSC-SMC gave rise to more foam cell formation than VSMCs did. Western blotting showed that treatment with 80 mg/L ox-LDL for 72 h resulted in significantly increased expression of SR-A and significantly decreased expressions of ABCA1 and caveolin-1.</p><p><b>CONCLUSIONS</b>Treatment of BMCS-SMCs with ox-LDL results in cholesterol ester accumulation in the cells to result in foam cells, the mechanism of which involves up-regulation of scavenger receptor SR-A expression and down-regulation of the reverse cholesterol transport protein ABCA1 and caveolin-1 expression.</p>