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目的:研究气虚血瘀证对BALB/c小鼠结肠癌人工血行转移的影响及相关机制。方法:将BALB/c小鼠随机分为4组,即空白对照组、血瘀组、肿瘤组和瘀加瘤组。于利血平血瘀造模的第15天经尾静脉接种肿瘤,第28天处死小鼠检测全血黏度、细胞外信号调节激酶1/2(ERK1/2)、基质金属蛋白酶2(MMP-2)及基质金属蛋白酶12(MMP-12)。结果:血瘀组及瘀加瘤组全血黏度均明显升高,与空白对照组比较差异极显著(P<0.01)。瘀加瘤组右肺转移灶计数明显高于肿瘤组,差异有显著性(P<0.05)。ERK1/2、MMP-2按血瘀组、肿瘤组、瘀加瘤组顺序梯度递增,与空白对照组比较差异显著(P<0.05)。MMP-12的表达在血瘀组减弱,瘀加瘤组增强,组间差异有显著性(P<0.05)。结论:气虚血瘀证能促进结肠癌转移,其作用机制可能是通过上调ERK1/2和MMP-2的表达,同时抑制MMP-12的表达来完成。
Objective: To study the effect and mechanism of qi deficiency and blood stasis syndrome on the hematopoietic metastasis of colon cancer in BALB / c mice. Methods: BALB / c mice were randomly divided into 4 groups: blank control group, blood stasis group, tumor group and stasis plus tumor group. The tumor was inoculated via the caudal vein on the 15th day in the model of reserpine stasis and the mice were killed on the 28th day to detect the whole blood viscosity, ERK1 / 2, MMP- 2) and matrix metalloproteinase 12 (MMP-12). Results: The whole blood viscosity of blood stasis group and stasis plus tumor group were significantly increased compared with the control group (P <0.01). The counts of right lung metastasis in the group of stasis plus tumor were significantly higher than those in the tumor group, the difference was significant (P <0.05). ERK1 / 2 and MMP-2 increased gradually with the order of blood stasis group, tumor group and stasis plus tumor group, compared with the blank control group (P <0.05). The expression of MMP-12 was weakened in blood stasis group and stasis plus tumor group, the difference was significant (P <0.05). Conclusion: Qi-deficiency and blood-stasis syndrome can promote the metastasis of colon cancer. Its mechanism may be through up-regulating the expression of ERK1 / 2 and MMP-2 and inhibiting the expression of MMP-12.