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. 2019 May 3;10:980. doi: 10.3389/fimmu.2019.00980

Figure 4.

Figure 4

PolyI:C inhibits ROS production in AP via the IFN-β/IFNAR-dependent signaling pathway. (A) 266-6 cells were stimulated with 0.5 mM taurocholate in the absence or presence of polyI:C (1 μg/ml), 24 h later, HO-1 protein levels in the cells were measured by western blotting; GAPDH was used as a loading control. (B) 266-6 cells were stimulated with 0.5 mM taurocholate in the absence or presence of IFN-β (200 U/ml), polyI:C (1 μg/ml), or IFNAR inhibitor (1 μM). Twenty-four hours later, HO-1 protein levels in the cells were measured by western blotting; GAPDH was used as a loading control. (C,D) 266-6 cells were stimulated with 0.5 mM taurocholate in the absence or presence of polyI:C (1 μg/ml) or IFN-β (200 U/ml), intracellular ROS was stained by DCFH-DA, and detected by fluorescence microscopy (C) and flow cytometry (D). Median fluorescence intensity (MFI) of stained DCFH-DA was calculated (D, right panel). (E–G) HO-1 protein expression levels in the pancreases from Saline, Caerulein-AP, and PolyI:C+Caerulein-A WT (E), Ifnb−/− (F), and Ifnar1−/− mice (G) were measured by western blotting; a non-specific (NS) band was shown as a loading control. Data of (A–C,E–G) are representative of three independent experiments. Data of (D), right panel are shown as mean ± SEM (n = 3). *p < 0.05, one-way ANOVA test.