Abstract | PURPOSE: METHODS: Fischer rats underwent 60 min of 70% partial hepatic ischemia. After 60 min of reperfusion, rat colon adenocarcinoma cells (RCN-H4) were inoculated intrasplenically. PSK was administered orally before I/R, after I/R, or before and after I/R. The weights of metastatic lesions of the liver or the numbers of liver metastatic nodules were determined on day 21. The effect of PSK on angiogenesis was studied by a rat cornea model using RCN-H4 cells or a vascular endothelial growth factor ( VEGF)-containing pellet and an in vitro VEGF-induced endothelial cell migration assay. RESULTS: PSK administration significantly (p < 0.05) suppressed the I/R-induced increase in hepatic metastasis of RCN-H4 cells. The suppression of I/R-promoted metastasis was observed irrespective of the timing of administration. Furthermore, PSK significantly suppressed angiogenesis induced by RCN-H4 cells (p < 0.05) and the VEGF pellet (p < 0.01). PSK significantly suppressed the VEGF-induced migration of vascular endothelial cells (p < 0.05). CONCLUSION: PSK may suppress metastasis induced by hepatic I/R. The suppression of angiogenesis by PSK may be one of the mechanisms of the inhibition of hepatic metastasis.
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Authors | Koji Tamagawa, Tetsuya Horiuchi, Tsutomu Wada, Kenji Bannai, Takao Ando |
Journal | Langenbeck's archives of surgery
(Langenbecks Arch Surg)
Vol. 397
Issue 3
Pg. 475-80
(Mar 2012)
ISSN: 1435-2451 [Electronic] Germany |
PMID | 22207390
(Publication Type: Journal Article)
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Chemical References |
- Immunologic Factors
- Proteoglycans
- Vascular Endothelial Growth Factor A
- polysaccharide-K
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Topics |
- Animals
- Cell Line, Tumor
- Colonic Neoplasms
(pathology)
- Disease Models, Animal
- Immunologic Factors
(therapeutic use)
- Liver Neoplasms
(physiopathology, secondary)
- Male
- Neovascularization, Physiologic
(drug effects)
- Proteoglycans
(therapeutic use)
- Rats
- Rats, Inbred F344
- Reperfusion Injury
(physiopathology)
- Stress, Physiological
(drug effects, physiology)
- Vascular Endothelial Growth Factor A
(metabolism)
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