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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. 2.

Fig. 2

β-FNA inhibition of IFNγ + HIV-1 Tat1–72-induced CXCL10 protein expression in normal human astrocytes is not affected by co-exposure to either naltrexone (Panel A) or CTAP (Panel B). Normal human astrocytes were exposed to human recombinant IFNγ (10 ng/ml) + HIV-1 Tat1–72 (100 nM) alone or in the presence of β-FNA (10 μM), naltrexone or CTAP (30 and 100 μM), or β-FNA + naltrexone or CTAP for 24 h. CXCL10 protein levels in the media were then measured by ELISA. The data are expressed as % control (relative to IFNγ + HIV-1 Tat1–72) and represent mean + S.E.M of 2–4 independent experiments; triplicate measures (wells) in each experiment. Data were analyzed using one-way ANOVA and Dunnett’s post test comparison. * p < 0.05 vs. IFNγ + HIV-1 Tat1–72