Skip to main content
. 2007 Feb 7;27(6):1422–1433. doi: 10.1523/JNEUROSCI.2382-06.2007

Figure 9.

Figure 9.

Aβ toxicity is JNK dependent and attenuated by ER-dependent estrogen actions. A, E2-induced neuroprotection against Aβ is ER dependent. Primary neuron cultures were pretreated with ICI 182,780 (ICI) at concentrations ranging from 0.01 to 10 μm for 60 min, followed by treatment with 0 nm (black bars) or 10 nm (gray bars) E2 for 60 min, and then exposed to 25 μm Aβ25–35 for 48 h. Controls groups with vehicle treatment (Veh), 10 nm E2 alone, and 1 μm ICI alone are shown in white bars. Data show mean cell viability (+SEM) from a representative experiment (n = 4). *p < 0.01 compared with E2 plus Aβ25–35 and 0 μm ICI treatments. B, Inhibition of JNK signaling reduces Aβ toxicity and increases estrogen neuroprotection. Neuron cultures were pretreated with 100 nm JNK inhibitor SP600125 (SP) for 60 min, followed by 10 nm E2 for 60 min, and then exposure to 25 μm Aβ25–35 for 48 h. Data show mean cell viability (+SEM) from a representative experiment (n = 4). Significance is defined as follows: #p < 0.01 compared with Aβ treatment; *p < 0.01 compared with E2 plus Aβ25–35 treatment.