Fig. 6

PPARγ agonists reverse HIV-1_ADA gp120-induced NF-κB (p-p65) phosphorylation in vivo. Adult Wistar rats were administered IP, 30 min prior to ICV bilateral injection of 4 μg/ventricle HIV-1_ADA gp120 with rosiglitazone (10 mg/kg). Saline (control) and gp120 (vehicle) animals received the same volume of DMSO/saline 1:10 IP. Hippocampus brain regions were isolated 5 h post ICV. For immunoblotting, hippocampus tissue nuclear extracts (50 μg) were resolved on a 10% SDS-polyacrylamide gel and transferred to a PVDF membrane. K-562 (immortalized myelogenous leukemia cell line) was used as a positive control for p-p65 protein. NF-κB (p-p65) was detected using a rabbit polyclonal p-p65^Ser536 (1:100 dilution). Actin was detected using a mouse monoclonal antibody (1:5000, dilution). Data generated from densitometric analysis is presented as a ratio of p-p65^Ser536 expression normalized to actin (loading control). Results are expressed as mean ± SEM relative to saline group (control) n = 3–4 animals/group. Asterisks and pound symbol represent data points significantly different from saline (control) and gp120 (vehicle) respectively (***p < 0.001, ###p < 0.001)