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Figure 2 | Comparative Hepatology

Figure 2

From: Low NO bioavailability in CCl4cirrhotic rat livers might result from low NO synthesis combined with decreased superoxide dismutase activity allowing superoxide-mediated NO breakdown: A comparison of two portal hypertensive rat models with healthy controls

Figure 2

Western blots of NOS isoforms. Liver homogenates of rats were used in Western blots; see Methods section. Normal rats (NL) were compared with prehepatic portal hypertensive rats, achieved by partial portal vein ligation (PPVL) and rats with carbon tetrachloride/phenobarbital induced (CCl4) cirrhosis. (A) Western blot of eNOS, representative of eight blots. Lane 1, marked with +: Human endothelial cells were used as positive control. Lanes 2–3: two different NL livers. Lanes 4–5: two different PPVL livers. Lanes 6–7: two different CCl4 cirrhotic livers. Prestained markers indicated the presence of 203, 120, 86, 52 kilodalton (kD) sized proteins. (B) Western blot of iNOS, representative of two blots. Lanes 1–2: two different NL livers. Lanes 3–4: two different PPVL livers. Lanes 5–6: two different CCl4 cirrhotic livers. Lane 7, marked with +: liver from a rat previously treated with lipopolysaccharide was used as positive control for iNOS (see Methods). Prestained markers indicated the presence of 130 and 86 kilodalton (kD) sized proteins. (C) Western blot of nNOS, representative of two blots. Lanes 1–2: two different NL livers. Lanes 3–4: two different PPVL livers. Lanes 5–6: two different CCl4 cirrhotic livers. Lane 7, marked with +: rat brain homogenate was used as positive control for nNOS (see Methods). Prestained markers indicated the presence of 130 and 86 kilodalton (kD) sized proteins.

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Comparative Hepatology

ISSN: 1476-5926