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.