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. Author manuscript; available in PMC: 2018 Feb 5.
Published in final edited form as: Shock. 2009 May;31(5):466–472. doi: 10.1097/SHK.0b013e31818ec47d

FIG. 3. Hypertonic saline significantly attenuates TNF-α–induced NF-κB nuclear localization.

FIG. 3

A, Immunofluorescent images show the intracellular localization of NF-κB. The nuclear stains (blue) are omitted from the bottom row. In unstimulated cells, most of the NF-κB p65 subunit (green) is sequestered in the cytoplasm (first column). Hypertonic saline pretreatment does not significantly change the intracellular location of the p65 subunit (second column). TNF-α causes the p65 subunit to accumulate in the nucleus at 30 min (third column). Hypertonic saline attenuates TNF-α– induced NF-κB nuclear translocation (fourth column) with more of the p65 subunit left within the cytoplasm. The orange bar equals 10 μm. All images acquired at 40 magnification. B, Hypertonic saline reduces nuclear NF-κB MFI. Nuclear staining was used to produce masks to measure the relative MFI of the p65 subunit within the nuclei. The MFI of HTS pretreatment–only cells are not different from controls. TNF-α causes a 4-fold increase that HTS reduces by more than 40%. Data from four separate experiments are presented as SEM. Both the TNF-α–only group and the HTS/TNF-α group are significantly different from all other groups (*#P < 0.001).