PKA Inhibitor H89 (N-[2-p-bromocinnamylamino-ethyl]-5-isoquinolinesulfonamide) Attenuates Synaptic Dysfunction and Neuronal Cell Death following Ischemic Injury

Figure 9

The measurement of AKT phosphorylation in Neuro2A cell against H/R injury. Western blotting experiments showed that the relative protein level of phosphorylation-AKT (p-AKT)/AKT significantly was increased in the H89 pretreatment group compared to the hypoxia and reperfusion group. β-actin was used as an internal control. Data were expressed as mean ± S.E.M, and each experiment included 4 repeats per condition. Differences were considered significant at . Normal: the normal control group, H/R: 4 hr hypoxia and 18 hr reperfusion injury group, H89: 2 hr PKA inhibitor H89 treatment group before 4 hr hypoxia and 18 hr reperfusion injury, and p-AKT: phosphorylation-AKT.