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. 2008 Jun 9;205(6):1491–1503. doi: 10.1084/jem.20071728

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© 2008 Cao et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jgp.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 1. — Deacetylase inhibitors decrease LPS activation of NO synthesis and NOS2 expression. (A) TSA inhibits LPS-induced NO production in a dose-dependent manner. RAW cells were pretreated with increasing amounts of TSA for 1 h, and then treated with or without LPS 100 ng/ml for 16 h, and the amount of NO₂⁻ was measured in the supernatant by the Griess reaction. (n = 3 ± the SD). (B) Sodium butyrate inhibits LPS-induced NO production in RAW cells. RAW cells were pretreated with increasing amounts of sodium butyrate for 1 h and treated with or without LPS 100 ng/ml for 16 h, and the amount of NO₂⁻ was measured in the supernatant by the Griess reaction (n = 3 ± the SD). (C) TSA inhibits the LPS-induced increase in NOS2 RNA levels (dose–response). RAW cells were pretreated with increasing amounts of TSA for 1 h and treated with LPS 100 ng/ml for 6 h. Total RNA was analyzed by Northern blotting with a cDNA probe for NOS2 (top) or a ribosomal phosphoprotein RNA 36B4 as a control (bottom). (D) TSA inhibits LPS-induced increase in NOS2 RNA levels (time course). RAW cells were pretreated with TSA 30 ng/ml for 1 h and treated with LPS 100 ng/ml for 0–7 h. Total RNA was analyzed by Northern blotting with a cDNA probe for NOS2. (E) TSA inhibits LPS-induced increase in NOS2 protein levels (dose–response). RAW cells were pretreated with increasing amounts of TSA for 1 h, LPS was added for 6 h, and cell lysates were immunoblotted with antibody to NOS2 (top) or ERα (bottom). (F) TSA decreases LPS-induced inflammatory cytokine RNA levels. RAW cells were treated with LPS and TSA for 4 h. Total RNA was analyzed by Northern blotting with probes for TNF-α, IL-1β, IL-6, or GAPDH as a control. (G) TSA decreases LPS-, PGN-, and poly(I:C)-induced NOS2 protein levels. RAW cells were treated with the TLR agonists PGN, poly(I:C), LPS, or E. coli for 16 h. Cell lysates were immunoblotted with antibody to NOS2. (H) TSA slightly increases expression of COX-2 and CXCL2. RAW cells were treated with LPS, TSA, or both as in F, and analyzed for COX-2 and CXCL2 expression by RT-PCR.