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

Figure 8

The measurement of PSD-95 expression in Neuro2A cells after H/R-induced injury. The level of PSD-95 was evaluated by immunocytochemistry. This image shows that the expression of PSD-95 in the H/R group was decreased compared to the normal group. PKA inhibitor H89 pretreatment increased the expression of PSD-95 in spite of hypoxia reperfusion injury. (b) Western blotting experiments showed that the relative protein expression of PSD-95 slightly increased in the H89 group compared to the hypoxia 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 and . Scale bar: 200 μm, PSD-95: green, 4′, 6-diamidino-2-phenylindole (DAPI): blue, normal: the normal control group, H/R: 4 hr hypoxia and 18 hr reperfusion injury group, and H89: 2 hr PKA inhibitor H89 treatment group before 4 hr hypoxia and 18 hr reperfusion injury.

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