Role of vascular cell adhesion molecule-1 in the mouse model of hepatic ischemia/reperfusion and the hematogenic metastasis.
- Author:
Yi LIU
1
;
Shang-lei NING
1
;
Yu-xin CHEN
1
;
Ke-sen XU
1
;
Nan-hai SHOU
1
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Liver; blood supply; Liver Neoplasms; pathology; Male; Mice; Mice, Inbred BALB C; Neoplasm Metastasis; Reperfusion Injury; complications; Vascular Cell Adhesion Molecule-1; physiology
- From: Acta Academiae Medicinae Sinicae 2014;36(4):426-431
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of ischemia/reperfusion (I/R) on tumor metastasis in a experimental mouse model of hematogenous metastasis after I/R and to quantify expression of vascular cell adhesion molecule-1 (VCAM-1) during I/R.
METHODSAn experimental mouse model of metastasis after partial hepatic I/R was designed to determine the effects of I/R on tumor metastasis to liver. Tumor loads were valued 14 days after operation. In addition, the expressions of alanine transaminase (ALT), aspartate transaminase (AST), and VCAM-1 were detected.
RESULTSTwo hours after hepatic reperfusion, ALT and AST levels in ischemia 45-minute group and ischemia 30-minute group were significantly higher than in the sham group (all P < 0.05). Also, the changes of ALT and AST were more obvious in the ischemia 45-minute group than in ischemia 30-minute group (all P < 0.05). In the sham group, both ALT and AST slightly and transiently increased. ALT and AST in the ischemia 45-minute group and ischemia 30-minute group at 8 hours were both significantly higher than those at 2 hours reperfusion (P<0.05). The tumor load (valued by hepatic replacement area) and the expression of VCAM-1 in ischemic lobe were significantly larger in the ischemia 45-minute group than in the ischemia 30-minute group and sham group (P = 0.013, P = 0.007). However, there was no statistical difference on tumor load between the right lobe of sham operated mice and the right lobe (nonischemic lobes) of mice subjected to I/R (P = 0.089). Mouse survivals were significantly longer in the sham group than in the ischemia 30-minute group (P = 0.041) but were not significantly different between the ischemia 45-minute group and ischemia 30-minute group (P = 0.055). VCAM-1 expression in ischemia 45-minute group was significantly higher than in ischemia 30-minute group and sham group(P = 0.003, P < 0.001), and it was positively correlated with the hepatic replacement area (r = 0.491, P = 0.045).
CONCLUSIONHepatic I/R promotes liver hematogenic metastasis of hepatocellular carcinoma in mice and at least in part, through the induction of VCAM-1 expression.
