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Fig. 8. NF{kappa}B activation is pro-apoptotic following UV and TNF-{alpha} treatments, while anti-apoptotic following pervanadate and H/R treatments. HeLa cells were infected with either Ad.BglII or Ad.I{kappa}B{alpha}AS at an MOI of 1000 particles/cell for 24 hours. Cells were treated with (A) UV (50 J/m2), (B) TNF-{alpha} (10 ng/ml), (C) pervanadate (50 µM) and (D) H/R (5 hours hypoxia, 18 hours reoxygenation) then harvested 18 hours after treatment. Cells are then trypsinized and stained with annexin-V-FITC and propidium iodine. Results depict the mean (±s.e.m., n=3) percent of apoptotic cells as shown by FACS analysis. Following UV and TNF-{alpha} treatment, I{kappa}B{alpha}AS expression significantly (P<0.01) increased apoptosis compared with the Ad.BglII-infected control group. By contrast, following pervanadate and H/R treatments, I{kappa}B{alpha}AS expression significantly decreased (P<0.01) the percentage of apoptotic cells as compared to the Ad.BglII-infected control group.





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