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. Author manuscript; available in PMC: 2015 Feb 1.
Published in final edited form as: Diabetologia. 2013 Nov 8;57(2):413–423. doi: 10.1007/s00125-013-3101-z

Fig. 6.

Fig. 6

Fig. 6

TXNIP is required for palmitate-induced NLRP3 inflammasome activation in HRE cells. (a) Representative blot and quantification of immunoprecipitation (IP) with TXNIP and blotting (IB) with NLRP3 after incubation with 100 μmol/l PN alone, 400 μmol/l palmitate alone (Pal-BSA) or both (Pal-BSA+PN). There was a higher association of TXNIP with NLRP3 in Pal-BSA and Pal-BSA+PN treatments only. n= 4; *p<0.05 vs BSA. Representative blots (b) and western blot analysis of TXNIP (c), NLRP3 (d) and cleaved caspase-1 (Casp-1) (e) in HRE cells transfected with either 0.6 μmol/l scrambled siRNA (SC) or Txnip siRNA after incubation with PN alone, Pal-BSA alone or both (Pal-BSA+PN) in comparison with control BSA in the SC group. TXNIP knockdown resulted in abrogation of the Pal-BSA-mediated activation of cleaved caspase-1. Two-way ANOVA showed significant interaction between PN and Pal-BSA in the combined Pal-BSA+PN group for cleaved caspase-1 expression in the SC group. Protein levels were normalised to α-tubulin and SC BSA control. n=3 or 4; *p<0.05 vs SC BSA; p<0.05 vs SC Pal-BSA p<0.05 vs SC PN-BSA; §p<0.05 vs all SC groups