Skip to main content
Fig. 10 | Molecular Brain

Fig. 10

From: Inhibition of autophagy by CRMP2-derived peptide ST2-104 (R9-CBD3) via a CaMKKβ/AMPK/mTOR pathway contributes to ischemic postconditioning-induced neuroprotection against cerebral ischemia-reperfusion injury

Fig. 10

Role of CaMKKβ in the ST2-104-mediated decline in apoptosis. SH-SHY5Y cells were treated with 20 mM glutamate plus 20 μM glycine or control medium or with ST2-104 peptide for 24 h at 37 °C and then apoptosis levels and apoptosis-related proteins were assessed. In some wells, 10 μM STO-609, an inhibitor of CaMKKβ was added for 24 h. a Apoptosis level was evaluated using the Hoechst 33,258 staining. Scale bar: 50 μm. For each well, at least 5 different fields were examined – a representative is shown here. b Detection of Bax, Bcl-2 and C-caspase-3 protein expression levels using Western blot analysis. Representative blots are shown. Levels of β-actin protein were used as the loading control. Bar represents mean ± SEM from 3 separate wells. **P < 0.01, vs. Con group; ##P < 0.01, vs. Glu group; $P < 0.05, vs. Glu + ST2-104 peptide group with one-way ANOVA with Tukey’s post-hoc test

Back to article page