Figure 4.

Gliotoxin attenuates NF-κB activation in experimental glomerulonephritis. A: Nuclear proteins from untreated nephritic, gliotoxin-treated, and control rats were analyzed by EMSA. Competition (c) with an excess of unlabeled probe was used as negative control. Specific NF-κB bands were densitometered, and data are expressed as increase versus control rats (▪, untreated nephritis; □, gliotoxin-treated; *, P < 0.05 versus nephritis). B–E: In situ localization of activated NF-κB in renal tissues. Control rats receiving gliotoxin (B) presented a weak staining. Nephritic animals presented a strong NF-κB activation in glomerular and tubular cells at day 4 (C), that was attenuated by gliotoxin treatment (D). Specificity of DNA-protein interaction in nephritic rats (same sample as C) was determined by competition with a 200-fold excess of unlabeled oligonucleotide (E). Original magnifications, ×200.