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. 2021 Mar 1;21(5):451. doi: 10.3892/etm.2021.9880

Figure 4.

Figure 4

Effect of FK18 on Akt, Erk phosphorylation and apoptosis-associated proteins in SH-SY5Y cells. (A) Representative western blot image demonstrating the effect of FK18 on p-Akt and p-Erk expression following the induction of glutamate in a time-dependent manner. (B and C) Semi-quantification of the relative expression of p-Akt/total Akt and p-Erk/total Erk following glutamate injury in a time-dependent manner. (D) Representative western blot image demonstrating the effect of FK18 on p-Akt and p-Erk expression in the presence or absence of LY294002 or U0126. (E and F) Semi-quantification of the relative expression of p-Akt/total Akt and p-Erk/total Erk in the presence or absence of LY294002 and U0126. (G) Cell viability of SH-SY5Y cells following glutamate injury in the presence or absence of LY294002 or U0126, as determined by MTS assay. (H) Representative western blots demonstrating the expression of Bcl-2, Bax and caspase-3 following glutamate injury, with or without FK18 pretreatment, in the presence or absence of LY294002 or U0126. (I) Bcl-2/Bax protein expression ratio following various treatments. (J) Semi-quantification of cleaved caspase-3 protein expression expressed as a ratio full length caspase-3 expression. The data is expressed as the mean ± SD. *P<0.05 and **P<0.01 vs. control group; #P<0.05 and ##P<0.01 vs. glutamate group; $P<0.05 and $$P<0.01 vs. glutamate-plus-FK18 group. Control group, treated with normal saline; Glu, glutamate; bFGF, basic fibroblast factor; PI, propidium iodide; p, phosphorylated; LY294002, Akt pathway inhibitor; U0126, Erk pathway inhibitor.