IndraLab
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"Inhibition of ATP-induced ASC speck formation by (C) Disulfiram 5 μM and (D) 10 μM. Nuclei are counterstained with DRAQ5 (red) (Original magnification x20) (E) Dosedependent inhibition of ATP-induced ASC-speck formation (relative activity in % in relation to maximal ASC-formation achieved by ATPstimulation of controls) by disulfiram (red curve) in the murine macrophage reporter cell line."
reach
"In the following selectivity screen, we observed a significant in- Analogously to the murine reporter cell screening and IC50 delineation process, IC50 values of hit compounds were also assessed in human cells using THP1 ASC-GFP reporter monocytes for the assessment of ASC speck formation and human primary monocytes for inhibition of IL-1β and IL-18 secretion.In line with the murine data, we could observe a dose-dependent inhibition of ATP-induced ASC speck formation by disulfiram in the human THP1 ASC-GFP reporter monocytes ( Figure 1F) ."
reach
"All compounds including the previously reported inflammasome inhibitor MCC950 14 as positive control and vehicle (DMSO) as negative control, were screened for activity at 10 μM concentration for inhibition of ATP-induced ASC speck formation in the ASC-mCerulean reporter cell line using a fully automated microscope (ArrayScan, Cellomics Inc.)."
reach
"The PKA inhibitor H89 increased the ASC speck formation induced by ATP, and it could partly reversed the inhibitory effect of baicalin on ATP induced ASC speck formation, further confirming that PKA signaling had been involved in the action of baicalin on suppressing NLRP3 inflammasome activation."