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首页> 外文期刊>World Journal of Gastroenterology >Antithrombin reduces reperfusion-induced hepatic metastasis of colon cancer cells.
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Antithrombin reduces reperfusion-induced hepatic metastasis of colon cancer cells.

机译：抗凝血酶可减少再灌注诱导的结肠癌细胞的肝转移。

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AIM: To examine whether antithrombin (AT) could prevent hepatic ischemia/reperfusion (I/R)-induced hepatic metastasis by inhibiting tumor necrosis factor (TNF)-alpha-induced expression of E-selectin in rats. METHODS: Hepatic I/R was induced in rats and mice by clamping the left branches of the portal vein and the hepatic artery. Cancer cells were injected intrasplenically. The number of metastatic nodules was counted on day 7 after I/R. TNF-alpha and E-selectin mRNA in hepatic tissue, serum fibrinogen degradation products and hepatic tissue levels of 6-keto-PGF(1alpha), a stable metabolite of PGI2, were measured. RESULTS: AT inhibited increases in hepatic metastasis of tumor cells and hepatic tissue mRNA levels of TNF-alpha and E-selectin in animals subjected to hepatic I/R. Argatroban, a thrombin inhibitor, did not suppress any of these changes. Both AT and argatroban inhibited I/R-induced coagulation abnormalities. I/R-induced increases of hepatic tissue levels of 6-keto-PGF(1alpha) were significantly enhanced by AT. Pretreatment with indomethacin completely reversed the effects of AT. Administration of OP-2507, a stable PGI2 analog, showed effects similar to those of AT in this model. Hepatic metastasis in congenital AT-deficient mice subjected to hepatic I/R was significantly increased compared to that observed in wild-type mice. Administration of AT significantly reduced the number of hepatic metastases in congenital AT-deficient mice. CONCLUSION: AT might reduce I/R-induced hepatic metastasis of colon cancer cells by inhibiting TNF-alpha-induced expression of E-selectin through an increase in the endothelial production of PGI2. These findings also raise the possibility that AT might prevent hepatic metastasis of tumor cells if administered during the resection of liver tumors.
机译：目的：探讨抗凝血酶（AT）是否能通过抑制大鼠肿瘤坏死因子（TNF）-α诱导的E-选择素表达来预防肝缺血/再灌注（I / R）诱导的肝转移。方法：通过夹住门静脉和肝动脉的左分支，在大鼠和小鼠中诱导肝I / R。脾内注射癌细胞。在I / R后第7天计算转移性结节的数量。测量了肝组织，血清纤维蛋白原降解产物和肝组织中6-酮-PGF（1alpha）（一种稳定的PGI2代谢产物）的TNF-α和E-选择素mRNA。结果：AT抑制了肝I / R动物的肿瘤细胞肝转移的增加以及TNF-α和E-选择素的肝组织mRNA水平。凝血酶抑制剂Argatroban不能抑制任何这些变化。 AT和阿加曲班均抑制I / R诱导的凝血异常。 I / R诱导的6-酮-PGF（1alpha）肝组织水平的增加被AT明显增强。消炎痛预处理可完全逆转AT的作用。在这种模型中，稳定的PGI2类似物OP-2507的给药显示出与AT类似的效果。与野生型小鼠相比，先天性AT缺陷型肝I / R小鼠的肝转移明显增加。 AT的使用显着减少了先天性AT缺陷小鼠的肝转移数量。结论：AT可能通过增加PGI2的内皮生成来抑制TNF-α诱导的E-选择素表达，从而减少I / R诱导的结肠癌细胞的肝转移。这些发现还增加了AT在肝肿瘤切除术中预防肝细胞转移的可能性。

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