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. 2015 Jan 13;16(1):1736–1754. doi: 10.3390/ijms16011736

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© 2015 by the authors; licensee MDPI, Basel, Switzerland.

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

AP7Glu inhibited lipopolysaccharide (LPS)-induced cell inflammation in RAW 264.7 cells. Raw cells were pre-treated with different concentrations of AP7Glu from 10, 5, 2.5, 1.25, 0.63, 0.31, 0.16 μM, or 0 μM (referred as (−)) for 1 h prior to the addition of 100 ng/mL LPS for 24 h. (A) The structure of AP7Glu is shown; (B) the percentage of cell viability was determined by ELISA; (C) The supernatants were harvested and NO production was quantified using ELISA. The data were presented as mean ± SD for the three different experiments performed in triplicate. ^### compared with sample of control group (one-way ANOVA followed by Scheffe’s multiple range tests). ** p < 0.01, and *** p < 0.001 were compared with LPS-alone group.

AP7Glu inhibited lipopolysaccharide (LPS)-induced cell inflammation in RAW 264.7 cells. Raw cells were pre-treated with different concentrations of AP7Glu from 10, 5, 2.5, 1.25, 0.63, 0.31, 0.16 μM, or 0 μM (referred as (−)) for 1 h prior to the addition of 100 ng/mL LPS for 24 h. (A) The structure of AP7Glu is shown; (B) the percentage of cell viability was determined by ELISA; (C) The supernatants were harvested and NO production was quantified using ELISA. The data were presented as mean ± SD for the three different experiments performed in triplicate. ^### compared with sample of control group (one-way ANOVA followed by Scheffe’s multiple range tests). ** p < 0.01, and *** p < 0.001 were compared with LPS-alone group.