Fig. 8
VI-16 inhibited Txnip mediated NLRP3 inflammasome activation by resisting oxidative stress. a Immunoblot analysis of IL-1β in supernatants (SN) and caspase-1, Txnip in extracts (Input) of LPS-primed differentiated THP-1 cells transfected with siRNA with scrambled sequence or siRNA specific for Txnip. b Immunoblot analysis of differentiated THP-1 cells transfected with siRNA with scrambled sequence (−) or siRNA specific for Trx-1. c ELISA of IL-1β in supernatants of LPS-primed differentiated THP-1 cells, transfected with Txnip siRNA, treated with 10 μM of VI-16, followed by treating for 1 h with ATP (5 mM), 3 h with nigericin (4 μM) and 6 h with MSU (150 µg/ml). Data are presented as mean ± SD. *P < 0.05, **P < 0.01 compared with scramble+DMSO group. d Level of ROS was measured in LPS-primed differentiated THP-1 cells treated with 5 mM of NAC for different time, followed by treating for 1 h with ATP (5 mM). e Immunoblot analysis of Txnip immunoprecipitates in LPS-primed differentiated THP-1 cells treated with 5 mM of NAC for different time, probed for Trx-1, NLRP3, and Txnip. f Immunoblot analysis of IL-1β in supernatants (SN) and extracts (Input) of LPS-primed differentiated THP-1 cells treated with 5 mM of NAC for different time. g Level of ROS was measured in LPS-primed differentiated THP-1 cells treated with 10 μM of VI-16, followed by treating for 6 h with H2O2 (10 mM) or rotenone (10 mM). Data are presented as mean ± SD. *P < 0.05. h Immunoblot analysis of IL-1β in supernatants (SN) and caspase-1 in extracts (Input) of LPS-primed differentiated THP-1 cells treated with 10 μM of VI-16, followed by treating for 6 h with H2O2 (10 mM) or rotenone (10 mM)
