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

Figure 3.

Figure 3

Baicalein inhibited TLR4/MyD88 signaling molecules in vivo and in vitro. (A) Mice were sacrificed at the end of the study, and total protein from the colon tissues was subjected to immunoblotting with antibodies against TLR4, MyD88, NF-κB p65, p-p65, IκBα, p-IκBα, p-38, p-p38 (1:1000 dilution) and β-actin (1:2000 dilution). One representative blot was shown. (B) Quantification of the protein expression was performed by densitometric analysis of the blots. (C) RAW264.7 cells were exposed to baicalein (0, 5, 10, 25, 50, 75, 100, 150 and 200 μM) for 48 h. Cell viability was determined using a CCK-8 assay kit. (D) RAW264.7 cells were treated with baicalein (0, 10, 25, 50 μM) for 2 h followed by an additional treatment with or without LPS (1 μg/ml) for 24 h. Total protein was extracted and subjected to immunoblotting with antibodies against TLR4, MyD88, p-IRAK-1, COX-2 (1:1000 dilution) and β-actin (1:2000 dilution). One representative blot was shown. (E) Quantification of the protein expression was performed by densitometric analysis of the blots. Expression was normalized to β-actin. Data were expressed as mean ± SD of three independent experiments (n = 3). ##p < 0.01, ###p < 0.001 vs. vehicle-treated group; *P < 0.05, **p < 0.01, ***P < 0.001 vs. TNBS/LPS-treated group.