Fig. 8: AST pretreatment decreased the phosphorylation levels of PI3K, Akt, and mTOR in the AD cells group.
From: Neuroprotective effect of astragalin via activating PI3K/Akt-mTOR-mediated autophagy on APP/PS1 mice
A Protein-protein interaction analysis of differently expressed autophagy-associated proteins using STRING database. B Representative bands of PI3K, p-PI3K, Akt, p-Akt, mTOR, and p-mTOR by WB detection in the HT22 cells. C–E Statistical analysis of p-PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR in HT22 cells. Data were presented as mean ± SD, n = 3/group. **p < 0.01 vs control group, #p < 0.05 and ##p < 0.01 vs AD group, @@p < 0.01 vs AST + AD group. F, G The expression levels of PI3K, p-PI3K, Akt, p-Akt, mTOR, and p-mTOR were detected by WB after the addition of Baf A1 or CQ in AD cell model. H, I Statistical analysis of p-PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR in HT22 cells of each group. Data were presented as mean ± SD, n = 3/group. *p < 0.05, ***p < 0.01 and ***p < 0.001 vs AST + AD group. J The expression levels of LC3BII/LC3BI and p62 were detected by WB after the addition of MK2206 or rapamycin in Aβ25-35-injured HT22 cells. K, L Statistical analysis of the corresponding LC3BII/LC3BI and p62 protein bands. Data were presented as mean ± SD, n = 3/group. *p < 0.05, **p < 0.01 vs AD group.
