Forty male Wistar rats were randomly divided into four experimental groups (n = 10 in each): (A) Control group (the
sham operation group); (B) I/R group (pretreated with
normal saline); (C) Small-dose (10 microg/kg) VnA pretreatment group; (D) Large-dose (20 microg/kg) VnA pretreatment group. Hepatic
ischemia/reperfusion (Hepatic I/R) was induced by occlusion of the portal vein and the hepatic artery for 90 min, followed by reperfusion for 240 min. The pretreatment groups were administered with VnA intraperitoneally, 30 min before surgery, while the control group and I/R group were given equal volumes of
normal saline.
Superoxide dismutase (SOD) activity,
myeloperoxidase (MPO) activity and
nitric oxide (NO) content in the liver tissue at the end of reperfusion were determined and liver function was measured. The expression of
intercellular adhesion molecule-1 (ICAM-1) and
E-selectin (ES) were detected by immunohistochemical examinations and Western blot analyses.
RESULTS: The results showed that hepatic I/R elicited a significant increase in the plasma levels of
alanine aminotransferase (ALT: 74.53 +/- 2.58 IU/L vs 1512.54 +/- 200.76 IU/L, P < 0.01) and lactic
dehydrogenase (LDH: 473.48 +/- 52.17 IU/L vs 5821.53 +/- 163.69 IU/L, P < 0.01), as well as the levels of MPO (1.97 +/- 0.11 U/g vs 2.57 +/- 0.13 U/g, P < 0.01) and NO (69.37 +/- 1.52 micromol/
g protein vs 78.39 +/- 2.28 micromol/
g protein, P < 0.01) in the liver tissue, all of which were reduced by pretreatment with VnA, respectively (ALT: 1512.54 +/- 200.76 IU/L vs 977.93 +/- 89.62 IU/L, 909.81 +/- 132.76 IU/L, P < 0.01, P < 0.01; LDH: 5821.53 +/- 163.69 IU/L vs 3015.44 +/- 253.01 IU/L, 2448.75 +/- 169.4 IU/L, P < 0.01, P < 0.01; MPO: 2.57 +/- 0.13 U/g vs 2.13 +/- 0.13 U/g, 2.07 +/- 0.05 U/g, P < 0.01, P < 0.01; NO: 78.39 +/- 2.28 micromol/
g protein vs 71.11 +/- 1.73 micromol/
g protein, 68.58 +/- 1.95 micromol/
g protein, P < 0.05, P < 0.01). The activity of SOD (361.75 +/- 16.22 U/mg
protein vs 263.19 +/- 12.10 U/mg
protein, P < 0.01) in the liver tissue was decreased after I/R, which was enhanced by VnA pretreatment (263.19 +/- 12.10 U/mg
protein vs 299.40 +/- 10.80 U/mg
protein, 302.09 +/- 14.80 U/mg
protein, P < 0.05, P < 0.05). Simultaneously, the histological evidence of liver
hemorrhage, polymorphonuclear neutrophil infiltration and the overexpression of
ICAM-1 and
E-selectin in the liver tissue were observed, all of which were attenuated in the VnA pretreated groups.
CONCLUSION: