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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. 3.

Fig. 3

IFNγ + HIV-1 Tat1–72-induced CXCL10 protein expression in normal human astrocytes is NF-κB- dependent. CXCL10 expression was induced in normal human astrocytes by stimulating with human recombinant IFNγ (10 ng/ml) + HIV-1 Tat1–72 (100 nM) for 24 h. To assess the role of NF-κB, the inhibitor of NF-κB nuclear translocation, 50 μM SN50 (or 50 μM of the inactive control peptide, SN50 Mut), was added to cell cultures 1 h prior to stimulation. The data represent mean + S.E.M of 2 independent experiments; triplicate measures (wells) in each experiment. Data were analyzed using one-way ANOVA and Newman-Keuls post test comparison. * p < 0.05 vs. IFNγ + HIV-1 Tat1–72