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. 2017 Nov 27;7:16374. doi: 10.1038/s41598-017-12562-6

Figure 5.

Figure 5

Baicalein inhibited MAPK signaling molecules in RAW264.7 cells and inhibited NLRP3 inflammasome activation in THP-1 cells. Cells were treated with baicalein for 2 h followed by an additional treatment with or without LPS (1 μg/ml) for 24 h. (A) Protein levels in RAW264.7 cells were determined with antibodies against JNK, p-JNK, ERK1/2, p-ERK1/2, p38, p-p38 (1:1000 dilution) and β-actin (1:2000 dilution) by immunoblotting. Quantification of the protein expression was performed by densitometric analysis of the blots. The ratio of phosphorylated MAPK to regular MAPK was shown (B). (C) Protein levels in THP-1 cells were determined with antibodies against NLRP3, ASC, caspase-1 (1:1000 dilution) and β-actin (1:2000 dilution) by immunoblotting. Quantification of the protein expression was performed by densitometric analysis of the blots (D). (E) THP-1 cells were pretreated with baicalein for 2 h and then followed by stimulation with ATP (5 mM) for 24 h. Protein expression was determined with antibodies against NLRP3, IL-1β (1:1000 dilution) and β-actin (1:2000 dilution) by immunoblotting. Quantification of the protein expression was performed by densitometric analysis of the blots (F). Expression was normalized to β-actin. Results were expressed as means ± SD of three independent experiments (n = 3). #p < 0.05, ###p < 0.001 vs. vehicle-treated group; *p < 0.05, **p < 0.01, ***P < 0.001 vs. LPS/ATP-treated group.