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. 2022 Feb 9;477(5):1329–1338. doi: 10.1007/s11010-022-04369-5

Fig. 4.

Fig. 4

Treatment of TAK inhibitor ameliorates TGF-β-induced NLRP3 inflammasome priming and activation pathways. LX-2 cells were untreated (―) or pre-treated with 50 nM of (5Z)-7-oxozeanol for 1 h and then treated with 10 ng/ml of TGF-β1 for 10 min in the presence of (5Z)-7-oxozeanol. Cell lysates were prepared, and protein expression levels associated with NLRP3 priming and secondary activation were analyzed by western blotting. GAPDH and NF-κB were used as the internal controls. a Representative western blot of NLRP3 priming-associated protein (left panel) and densitometric quantification are shown (right panel). b Representative western blots of NLRP3 activation-associated protein (left panel) and densitometric quantification are shown (right panel). **p < 0.01, *p < 0.05 vs. CON; ###p < 0.005 vs. TGF-β (n = 3/group)