Effects of Bee Venom on Glutamate-Induced Toxicity in Neuronal and Glial Cells
Figure 3
BV suppresses the activation of glutamate-mediated signaling in N2a neuronal cells. To determine the mechanism by which BV protects against glutamate-induced cell toxicity, N2a cells were preincubated with 2.5 μg/mL BV for 30 min prior to treatment with 5 mM glutamate for 30 min. (a) Total cell lysates were separated using 10% SDS-PAGE and western blots were performed using antiphospho JNK or JNK antibodies. (b) Glutamate-induced p38 activation was determined by anti-pp38 antibody. (c) The expression level of phospho-ERK was investigated with anti-pERK antibody. (d) The expression of phospho-Akt was measured with antiphospho-Akt antibody in N2a cells. (e) Levels of tubulin were measured to control for protein loading. Immune blots were quantified with the relative phospho-/nonphospho- ratio as indicated. *, **, and *** indicate P < 0.05, P < 0.005, and P < 0.001, respectively, compared to untreated cells. ## indicates P < 0.005 compared to glutamate-treated N2a cells (Glu). Con: control, BV: BV-treated cell, Glu: glutamate-treated cell, and BV+Glu: BV pretreated-cells prior to glutamate treatment.
