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Fig. 4 | Molecular Brain

Fig. 4

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. 4

Prevention of excitotoxic death with 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 or 48 h at 37 °C and then cell viability was evaluated with the MTT assay. Cell viability was measured with the indicated concentrations of ST2-104 peptide for 24 h (a) and 48 h (b). (c), (d) Cell viability was measured with indicated concentration of Glu treatment for 24 h (c) and 48 h (d). e Cell viability was measured with indicated concentration of ST2-104 peptide in Glu-triggered cells. Average death in each coverslip was counted in three fields. The percentage cell viability of 6 wells is represented as S.E. (error bars) (n = 6 for each condition). f The representative images of the cells after insult and treatment groups; scale bar, 50 μm.**P < 0.01, ***P < 0.001, ****P < 0.0001 vs. Con group; ##P < 0.01 vs. Glu group with one-way ANOVA with Tukey’s post-hoc test

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