Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2015 Sep 25;63(1-3):228–235. doi: 10.1007/s12026-015-8692-7

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2015

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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.

PMC Copyright notice

Fig. 4 — 2AP suppresses poly(I:C)-induced IL-36γ release, while 7DG has no effect on release. a Cells were stimulated for 96 h with 1500 ng/ml poly(I:C) ± the broad spectrum PKR inhibitor 2AP (1 mM) or the more specific inhibitor 7DG (5 μM), and IL-36γ accumulation in the conditioned medium measured by ELISA. Bars show mean ± SD of 5 experiments (*p < 0.001 compared to control cells treated with solvent, **p < 0.001 compared to cells treated with poly(I:C) but no inhibitor). b Cells were treated for 96 h with 1500 ng/ml poly(I:C) ± 2AP at the concentrations shown, and intracellular IL-36γ levels determined by western blot with β-actin as a loading control. A representative blot is shown. c Cells were treated with 2 μM poly(I:C) ± 5 μM 7DG for 96 h and the culture medium assayed for released lactic dehydrogenase (LDH) as a measure of cell death. 7DG suppressed the elevated cell death induced by high-dose poly(I:C) (*p < 0.001)