Research Paper Volume 12, Issue 13 pp 13187—13205

Figure 7. The proposed scheme for the possible mechanism of EA pretreatment suppresses CIR-induced autophagy via the SIRT1-FOXO1 signaling pathway. EA pretreatment at GV20, LI11, and ST36 significantly alleviated neurological deficits, reduced infarct volume, increased the dendritic spine density of cortical neurons, decreased the LC3-II/LC3-I ratio, and up-regulated p62 level. The above beneficial effects may be achieved by the activation of SITR1 and the inhibition of acetylation of FOXO1, as well as the suppression of Atg7 expression and the interaction of Ac-FOXO1 and Atg7.