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. 2019 Jul 24;25:5482–5492. doi: 10.12659/MSM.915251

Figure 6.

Figure 6

AKT antagonist and AKT agonist contributed to upregulating p-AKT, PI3K, and apoptosis-associated proteins expression in HGC cells after infection. (A) For AKT inhibitor. (B) For AKT agonist. When the groups were pretreated with AKT antagonist MK-2206, the expression of the Bax/Bcl-2 and cleaved caspase 3 proteins increased in HGC cells compared with cells without AKT antagonist (** P<0.01). The expression of the Bax/Bcl-2 and cleaved caspase 3 proteins decreased significantly (** P<0.01) in cells with AKT agonist IGF-1 treatment compared with cells without pretreatment. On the other hand, the expression of PI3K and p-AKT proteins decreased in AKT antagonist-pretreated groups (** P<0.01), but increased in AKT agonist-pretreated groups (** P<0.01).