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. 2019 Jan 1;8(1):17. doi: 10.3390/cells8010017

Figure 2.

Figure 2

Inhibition of S1PR2 by its specific antagonist (JTE013) attenuated p-PI3K, p-ERK, p-JNK, p-p38, and p-NF-kBp65 protein expressions induced by Aa in BMMs. Murine BMMs were treated with either vehicle or JTE013 for 30 min. Then cells were either uninfected or infected with Aa for 4 h. (A) p-PI3K, p-ERK, p-JNK, p-p38, p-NF-κBp65, and control GPADH protein expressions were evaluated by western blot. (B) p-PI3K protein density, (C) p-ERK protein density, (D) p-JNK protein density, (E) p-p38 protein density, and (F) p-NF-κBp65 protein density were analyzed and normalized by GAPDH protein expression. (* p < 0.05, ** p < 0.01, *** p < 0.001).