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. 2004 Dec 15;114(12):1741–1751. doi: 10.1172/JCI18058

Figure 2.

Figure 2

Diabetes or AGE-albumin induces transcriptional activity of NF-κB in sciatic nerves. (A) NF-κB–controlled β-globin and β-actin transcription in sciatic nerves of healthy control mice (lanes 1–3) and diabetic mice (lanes 4–7) 6 weeks after induction of diabetes; bar graphs summarize the semiquantitative results (β-globin/β-actin ratio) obtained in all mice studied (black bar, control; gray bar, diabetes). The mean ± SD is reported; *P < 0.05. The number of mice studied was 4 for controls, 5 for diabetes. (B) β-Globin and β-actin transcription in sciatic nerves of diabetic mice with bad glycemic control (lane 1) and good glycemic control due to intensified insulin treatment (lane 2); n = 2 for each group. (C) β-Globin and β-actin transcription in sciatic nerves of healthy controls (lane 1) compared with mice that had had diabetes for 3 months, without (lane 2) and with sRAGE treatment (lane 3); n = 3 for each group. (D and E) β-Globin, NF-κBp65, and β-actin transcription in sciatic nerves of mice treated with native albumin (lane 1), AGE-albumin alone (lane 2), or AGE-albumin in the presence of sRAGE (D, lane 3), anti-RAGE IgG (RAGE-Ab; D, lane 4), or the antioxidant thioctic acid (TA; E, lane 3); n = 3 for each group. (F) IL-6 transcription in sciatic nerves studied in A–E from healthy (lanes 1 and 2) and diabetic (lanes 3–5) mice with bad (lanes 3 and 4) and good (lane 5) glycemic control and mice treated with native albumin (lane 6), AGE-albumin alone (lane 7), or AGE-albumin in the presence of sRAGE (lane 8), anti-RAGE IgG (lane 9), or thioctic acid (lane 10).