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. 2015 Mar 12;20(1):612–624. doi: 10.2119/molmed.2014.00156

Figure 1.

Figure 1

(A,B) Representative autoradiograph of Western blot analysis for supernatant HMGB1 levels in THP-1 cells treated with LPS in the presence or absence of DIQ (300 μmol/L), a PARP1 inhibitor (Figure 1A). Experiment was repeated by treating THP-1 cells with EB-47, a new potent PARP1 inhibitor and supernatant HMGB1 concentrations were analyzed (Figure 1B). THP-1 cells were treated with LPS (10 μg/mL) for 18 h. The gel is representative of three experiments with similar results. (C) Representative autoradiograph of Western blot analysis for supernatant HMGB1 levels in bone marrow–derived macrophages from WT and PARP1−/− treated with LPS. The gel is representative of three experiments with similar results. (D) Representative Western blot analysis for supernatant HMGB1 concentrations in naïve, nontarget siRNA and PARP1 siRNA transfected THP-1 cells treated with LPS. Cells were treated with LPS (10 μg/mL) for 18 h. The gel is representative of three experiments with similar results. (E) PJ-34 (10 mg/kg, IP, n = 10), or saline (IP, n = 10) was administered 3 h prior to CLP. CLP was performed and blood was collected 24 h later. Serum HMGB1 concentrations were measured by ELISA.