Downregulation of TNF-α/TNF-R1 Signals by AT-Lipoxin A4 May Be a Significant Mechanism of Attenuation in SAP-Associated Lung Injury

Figure 7

Inhibition of NF-κB/p65 activation in TNF-R2^(-/-) HPMECs and lung tissue by AT-Lipoxin A4. TNF-R2^(-/-) HPMECs were pretreated with AT-Lipoxin A4 (50 ng/mL) for 1 h and then stimulated with TNF-α (50 ng/mL) for 15 min. (a–c) Western blot assay shows expressions of nuclear NF-κB, cytoplasmic NF-κB, and total p-NF-κB in TNF-R2^(-/-) HPMECs. (d, e) Single and merged images show immunofluorescence staining of NF-κB (green) in lung tissue at 12 h or 24 h after the procedure. The cell nucleus is stained blue by DAPI. (f, g) Western blot assay shows expressions of total NF-κB in lung tissue at 12 h or 24 h after the procedure. Beta-actin and Lamin B were used as internal controls, respectively. The data showed representatives of at least three independent experiments. compared with the control, compared with TNF-α in the absence of AT-Lipoxin A4, and compared with TNF-α in the absence of AT-Lipoxin A4.

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