Edaravone Attenuated Particulate Matter-Induced Lung Inflammation by Inhibiting ROS-NF-κB Signaling Pathway

Figure 6

EDA attenuated PM-induced activation of NF-κB p65 signaling pathway. (a) HBECs were treated with 500 μM EDA and then stimulated with 300 μg/mL PM for 24 h. The phosphorylation of the NF-κB p65 signaling pathway was detected by western blot. The optical densities of phospho-NF-κB p65 are shown in (b). (c) Mice were intratracheally instilled with PM at 100 μg/day/mouse for 2 consecutive days. EDA (2, 10, or 20 mg/kg) was intraperitoneally injected prior to PM exposure for 1 h. The phosphorylation of NF-κB p65 in lung tissues was detected by western blot. The optical densities of phospho-NF-κB p65 are shown in (d). (e) The transfection efficiency of NF-κB siRNA was detected by RT-PCR. (f) The protein level of NF-κB was tested by western blot in HBECs which were transfected with NF-κB siRNA with or without PM exposure. The optical densities of phospho-NF-κB p65 are shown in (g). (h) The mRNA level of inflammatory factors IL-6, IL-1α, and IL-1β was detected by RT-PCR. or , compared with the control group; ^# or ^##, compared with the PM group; or 5. EDA: edaravone; PM: particulate matter; HBECs: human bronchial epithelial cells.

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