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. Author manuscript; available in PMC: 2014 Mar 1.
Published in final edited form as: Neurochem Int. 2013 Jan 31;62(4):478–485. doi: 10.1016/j.neuint.2013.01.013

Fig. 5.

Fig. 5

β-FNA inhibits IFNγ + HIV-1 Tat1–72, -induced p38 activation in normal human astrocytes. In the presence or absence or β-FNA (10 μM), normal human astrocytes were exposed to human recombinant IFNγ (10 ng/ml) + HIV-1 Tat1–72 for 10–270 min. Panel A): Western blot was used to determine levels of total p38 and phosphorylated-p38 (p-p38) in the cytosolic fraction. Panel B): Data for the densitometric analysis represent mean + S.E.M of 3–5 independent experiments. Integrated density values are presented as a ratio of p-p38/total p38 and expressed as fold change relative to unstimulated control.. Data were analyzed using one-way ANOVA and Newman-Keuls post test comparison. ** p < 0.01 vs. IFN γ + HIV- 1 Tat1–72 at 10 min; *** p < 0.001 vs. IFNγ + HIV-1 Tat1–72 at 30 min.