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

Figure 3

The measurement of neurite outgrowth in Neuro2A cells. (a) The graph of neurite outgrowth length (μm) in all groups. The neurite length significantly decreases in N2A cells against hypoxia reperfusion injury. Data are expressed as mean ± S.E.M. Significant intergroup differences were determined by one-way analysis of variance (ANOVA) followed by Bonferroni post hoc multiple-comparison test. Differences were considered significant at . (b) The image using bright field microscope in the normal group shows well developed neurite of N2A cells. (c) The image using bright field microscope in hypoxia reperfusion group shows shorter neurite outgrowth of N2A cells than the normal group. (d) The image using bright field microscope in H89 group shows well developed neurite of N2A cells compared to the hypoxia reperfusion group. Each experiment included 3 repeats per condition. H89 protected N2A cells against the neurite damage under H/R injury. 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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