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Fig. 12 | Molecular Brain

Fig. 12

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. 12

Involvement of a CaMKKβ/AMPK/mTOR pathway in the effects of ST2-104. 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 protein levels were assessed by immunoblotting. Detection of CaMKKβ, AMPK, pAMPK, mTOR and p-mTOR 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 < 0.05, ##P < 0.01, vs. Glu group; $P < 0.05, $$P < 0.01 vs. Glu + ST2-104 peptide group with one-way ANOVA with Tukey’s post-hoc test

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