Fig. 2 | Signal Transduction and Targeted Therapy

Fig. 2

From: Novel insights into stress-induced susceptibility to influenza: corticosterone impacts interferon-β responses by Mfn2-mediated ubiquitin degradation of MAVS

Fig. 2

CORT enhances susceptibility to influenza virus in mice. a, b Plasma CORT concentrations detected by HPLC-UV method in mice at different times post-restraint stress and in mice subcutaneously injected with CORT (1 and 2 mg/kg) for 2 d (n = 10). c Mice were subcutaneously injected with CORT (1 mg/kg) or GR antagonist RU486 (25 mg/kg) for 2 d, and then inoculated with H1N1 virus. The survival rate of virus-infected mice was monitored for 21 d (n = 10). d On the 4th day after H1N1 infection, NP gene expression in the lungs tissues were measured by RT-qPCR (n = 3). e NP protein expression and histological changes were analyzed by immunostaining (scale bar, 50 μm) and H&E staining (scale bar, 200 μm) in the lung sections, respectively. White arrows indicate the presence of inflammatory infiltrates. Green arrows indicate thickened alveolar wall. Blue arrow indicates hemorrhage exudate. f A549 cells were pretreated with CORT (100 μM) for 48 h, and then infected with H1N1 virus (10 TCID50). The viral titer was determined by TCID50 assay at 12 h post infection (n = 3). g, h the expression of NP gene and protein were measured by RT-qPCR and western blotting (n = 3). CORT, corticosterone; GR-Ant, glucocorticoids receptor antagonist (RU486). Data are expressed as mean ± SD. *P < 0.05, **P < 0.01 vs. Control group; #P < 0.05, ##P < 0.01 vs. Virus group; &P < 0.05 vs. “Stress+Virus” group; §§P < 0.01 vs. “CORT + Virus” group

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