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. 2008 Aug 15;283(33):22601–22611. doi: 10.1074/jbc.M800524200

FIGURE 8.

FIGURE 8.

2-AG protects hippocampal neurons from proinflammatory and excitotoxic insults. a1–a5, TUNEL images of hippocampal neurons in control (a1), IL-1β (50 ng/ml (a2)), IL-1β + 2-AG (1 μm (a3)), IL-1β + 2-AG (5 μm (a4)), and IL-1β + 2-AG (5 μm) + SR-1 (5 μm (a5)) for 24 h. a6, percentages of injured neurons under different treatments (n = 10–12). b1–b5, TUNEL images of hippocampal neurons in control (b1), Glu (50 μm (b2)), Glu + NS398 (20 μm (b3)), Glu + 2-AG (5 μm (b4)), and Glu + 2-AG (5 μm) + SR-1 (5 μm (b5)) for 24 h. b6, percentages of injured neurons under different treatments (n = 10). c1, Hoechst staining of hippocampal neurons in control, Glu (50 μm), Glu + NS398 (20 μm), Glu + 2-AG (3 μm), and Glu + 2-AG + SR-1 (5 μm) for 24 h. c2, percentages of apoptotic neurons under different treatments (n = 5). d, Western blot analysis of cleaved caspase-3 in control, Glu (50 μm), 2-AG (1 and 5 μm), and SR-1 (1 μm). e, glutamate elevates COX-2 expression, and 2-AG attenuates Glu-induced elevation of COX-2. Hippocampal neurons in culture were treated with Glu for 24 h in the absence and presence of 2-AG and 2-AG + SR-1. **, p < 0.01, compared with control; #, p < 0.05, and ##, p < 0.01 compared with IL-1β or glutamate.