Figure 4.
Effects of macrophage-inhibitory peptide TKP on gp120- and SDF-1-induced neuronal apoptosis and on astrocyte activation of immunologic NO synthase. (A) TKP protected neurons from gp120SF2 toxicity. (B) TKP did not protect neurons from SDF-1β toxicity. Experimental conditions and analysis of apoptosis as in the legend to Fig. 2, except TKP (50 μM) was used instead of β-chemokines. ∗, P < 0.01 compared with value for gp120 or SDF-1β. (C) As a control to show that TKP did not prevent astrocyte activation, TKP did not inhibit release of NO from cytokine-stimulated astrocytes in cultures depleted of macrophages/microglia (see Materials and Methods). Astrocytic iNOS was induced by treatment with the cytokines tumor necrosis factor α (200 units/ml), IFN-γ (200 units/ml), and IL-1β (1 ng/ml) for 24 hr in the presence or absence of TKP. “Control” indicates samples without TKP and cytokines. Nitrite levels were monitored in the culture medium as an index of NO release by astrocytes. ∗, P < 0.01 compared with value for control but not significantly different from each other.