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. 2017 Aug 10;7:7735. doi: 10.1038/s41598-017-05245-9

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Effect of HIV-1 Tat treatment on NF-kappaB activation in the nuclear extracts of frontal cortex and astrocytes activation. (a) The panel shows representative NF-kappaB activation complex bands in the different groups of rats. (b) The quantitative analysis revealed that intracolonic HIV-1 Tat administration yields to a significant increase of NF-kappaB, as compared to vehicle, lidocaine, or bisacodyl groups (OD = optical density in mm²). (c) HIV-1 Tat caused a marked increase of GFAP, S100B, TLR-4 and iNOS protein expression in the frontal cortex homogenates of treated rats. (d) Quantitative analysis reveled that HIV-1 Tat induced a significantly higher expression of GFAP, S100B, TLR-4 and iNOS, than lidocaine, or bisacodyl groups. (e,f) In the medium of frontal cortex homogenates deriving from HIV-1 Tat group a significant increase of NO₂ ⁻ and S100B was also observed as compared to the other groups. (Results are expressed as mean ± SEM; ***p < 0.001 vs all other groups; °°°p < 0.001 vs HIV-1 Tat group; n = 6 for each group).