Nephroprotective Effects of N-Acetylcysteine Amide against Contrast-Induced Nephropathy through Upregulating Thioredoxin-1, Inhibiting ASK1/p38MAPK Pathway, and Suppressing Oxidative Stress and Apoptosis in Rats

Figure 2

NACA inhibited CM-induced renal tubular cell apoptosis as detected by TUNEL staining and western blot analyses of cleaved caspase 3. CM increased the number of TUNEL-positive renal tubular cells (blue arrows), and pretreatment with NAC or NACA blocked this effect. TUNEL-stained kidney sections (magnifications ×200) from CON rats (a), CIN rats (b), NAC+CIN rats (c), NACA1+CIN rats (d), and NACA2+CIN rats (e). TUNEL-positive cells are marked by blue arrows. (f) Quantitative analysis of TUNEL-positive cell number. (g) Western blot analyses of cleaved capsase-3. (h) Relative densitometry analysis of the ratio of cleaved caspase 3 to beta-actin. Figures are representative of 5 to 8 rats from each group. The values are means ± SD (). versus CON, versus CON, versus CIN, and versus CIN+NAC.

(a)

(b)

(c)

(d)

(e)

(f)

(g)

(h)